1. Dr Imran.

2. • Largest organ in the body
• Wt – 1500 to 1600gms
• Reddish brown triangular pyramid shaped, in
rt. Hypochondrium and most of epigastrium.

3. Cystic artery
sole supply to bile
duct

4. liver
pancreas
spleen
Portal vein: 80%
Hepatic artery: 20%
Dual Blood Supply of Liver
Liver has dual blood
supply:
80% portal vein
20% hepatic artery

5.  For anatomically divided into 2 left and right
lobes with right being bigger.
 Functionally divided into lobes by the portal
vein into 8 lobes.
 Each lobe having a portal vein, branch of
hepatic artery and a bile canaliculi.

6.  The biliary system rt and lt hepatic ducts which
combine to form common hepatic duct drains
to the gall bladder by cystic ducts.
 Gall 9cm in length, capacity of 50ml, bld supply
from cystic artery, branch of hepatic artery.
 Sphincter of ODDI is at the duodenal opening.

7. It is connected to the diaphragm and abdominal
walls by five ligaments:
the membranous falciform (also separates the
right and left lobes),
coronary, right and left triangular ligaments,
and the fibrous round ligament (which is
derived from the embryonic umbilical vein).

8.  Anatomically the liver is divided into a
Right and a Left lobe by the falciform
ligament
 The Right lobe also has two minor lobes-
The caudate lobe and The quadrate lobe

11.  The Liver receives around 1500 ml of blood/min
 The blood supply of the Liver is derived from The
Portal Vein (80%) and The Hepatic Artery (20%)
 Terminal branches of the hepatic portal vein and
hepatic artery empty together and mix as they enter
sinusoids in the liver.
 Sinusoids are distensible vascular channels lined
with highly fenestrated endothelial cells and
bounded circumferentially by hepatocytes.

12. 12

13.  The blood leaves the sinusoids via a
central vein , which drains in the hepatic vein.

14. Claude Couinad
A French surgeon &
anatomist who made
significant contribution in
the field of hepatobiliary
surgery ,he was the first to
describe segmental
anatomy of the liver

15.  Middle hepatic vein divides the liver
into right and left lobes (or right and
left hemiliver). This plane runs from the
inferior vena cava to the gallbladder
fossa (Cantlie's line)
 Right hepatic vein divides the right
lobe into anterior and posterior
segments
 Left hepatic vein divides the left
lobe into a medial and lateral part.

17.  Liver lobules – hexagonal structures consisting of
hepatocytes
 At each of the six corners of a lobule is a portal triad

18. Portal Triads: Branches of two vessels: portal vein,
hepatic artery, along with bile drainage ductules all run
together to infiltrate all parts of liver.
Zonal Flow of Blood

19. Zone 1-
Rich in Oxygen, mitochondria
•Concerned with Oxidative metabolism and synthesis of
glycogen
Zone 2- transition
Zone 3-
• lowest in Oxygen, anaerobic metabolism,
•Biotransformation of drugs, chemicals, and toxins
•Most sensitive to damage due to
ischemia, hypoxia, congestion

20. Hepatic Micro Circulatory Cone

22. Regulation of Hepatic Blood Flow
Intrinsic Regulation
• Hepatic Arterial Buffer Response -HABR
• Pressure flow Autoregulation
• Metabolic control
Extrinsic Regulation
• Neural Control
• Humoral Control

23.  With an intact HABR, changes in portal venous flow
cause reciprocal changes in hepatic arterial flow.
Portal venous flow reduced then there is reduction in
hepatic artery resistance.
But not vice versa.
 The HABR mechanism involves the synthesis and
washout of adenosine from periportal regions.


24.  Various disorders (e.g., endotoxemia, splanchnic
hypo perfusion) may decrease or even abolish the
HABR and render the liver more vulnerable to
hypoxic injury.
 Factors increasing hepatic blood flow: feeding,
glucagon, hypercapnia, recumbent position,
hepatocellular enzyme induction, ac. Hepatitis.
 Factors decreasing: Anesthetic agents, surgical
trauma, IPPV, PEEP, bet adrenergic blockade,
Hypocapnia, Vasopressin.

25.  Hepatic pressure auto-regulation keeps constant blood flow
despite wide fluctuation in systemic BP. The mechanism
involves myogenic responses of vascular smooth muscle to
stretch.
 The hepatic artery exhibits pressure-flow auto regulation in
metabolically active liver (postprandial) but not in the fasting
state. Thus, hepatic flow autoregulation is not likely to be an
important mechanism during anesthesia.
 Pressure-flow autoregulation is nonexistent in the portal
circulation.Thus, decrease in systemic blood pressure—as
often occurs during anesthesia—typically lead to proportional
decrease in portal venous flow

26.  Decrease in oxygen tension or the pH , ↑ Pco2 of
portal venous blood ,typically lead to increase in
hepatic arterial flow.
 Postprandial hyperosmolarity increases hepatic
arterial and portal venous flow but not in the fasting
state.
 The underlying metabolic and respiratory status
(e.g., hypercapnia, alkalosis, arterial hypoxemia) also
modulates the distribution of blood flow within the
liver.

27.  Fibres of the vagus, phrenic and splanchnic nerves
(postganglionic sympathetic fibres from T6 to
T11)enter the liver at the hilum
 When sympathetic tone decreases, splanchnic
reservoir increases whereas sympathetic
stimulation,translocates blood volume from the
splanchanic reservoir to the central circulation.
 Vagal stimulation alters the tone of the
presinusoidal sphincters, the net effect is a
redistribution of intrahepatic blood flow without
changing total hepatic blood flow.

28.  Gastrin, Glucagon, Secretin, Bile
salts, Angiotensin
II, Vasopressin, Catecholamines.
Cytokines, Interleukins, and other
inflammatory mediators have been implicated
in the alteration of normal splanchnic and
hepatic blood flow.

29. INCREASE IN HEPATIC
BLOOD FLOW
DECREASE IN HEPATIC
BLOOD FLOW
 Hypercapnia
 Acute hepatitis
 Supine posture
 Food intake
 Drug: Beta Agonist
Phenobaritone
 Enzyme inducers
 IPPV
 Hypocapnia
 Hyhpoxia
 Cirrhosis
 alpha Stimulation
 Beta blocker
 Halothane, volatile &
anesthetics
 Vasopressin

30.  Liver is supplied by sympathetic nerve fibres (
T6 to T11).
 Parasympathetic fibres – Rt & Lt Vagus.
 Fibres from Rt Phrenic nerve.
 Some autonomic fibres synapse first with Celiac
Plexus whereas others reach the liver directly
via splanchnic nerves & vagal branches before
forming Hepatic Plexus

31. 1. Vascular functions
2. Metabolic functions
3. Bile formation & Excretion

32.  Normal Blood flow – 1500ml/min
 25 to 30% from Hepatic Artery
 70 – 75% from Portal veins.
 Hepatic Artery supplies 45 – 50% of liver’s oxygen
requirement
 Portal veins supplies the remaining 50 – 55%
 The total blood flow from this dual supply represents
25 – 30% of cardiac output

33.  Portal vein pressure only about 7 – 10mmHg but
the low resistance of hepatic sinusoids allows rel.
large blood flow through portal vein.
 Small changes in hepatic venous tone thus can
result in large changes in hepatic blood vol.,
allowing liver to act as a blood resevoir.

34. Hemorrhage
↓
Decrease in hep. Venous tone
↓
Blood shifts from hep. Veins & sinusoids into
central venous circulation & augments
circulating blood vol upto 300ml.

35.  Kupffer cells lining sinusoids are part of monocyte –
macrophage system.
 Func – phagocytosis, processing Ag, release of
various proteins, enzymes, cytokines & other chem.
Mediators.
 Phagocytic activity is responsible for removing
colonic bacteria & endotoxin entering bloodstream
from portal circulation.
 Cellular debris, viruses, proteins & particulate matter
in blood are phagocytosed

36. 1. Carbohydrate Metabolism
2. Protein Metabolism
3. Fat Metabolism
4. Drug Metabolism
5. Other Metabolic functions

37.  The final products of carbohydrate metabolism are
glucose, fructose & galactose.
 With exception of large amount of fructose that is
converted by liver to lactate, hepatic conversion of
fructose & galactose into glucose makes glucose
metabolism final common pathway for most
carbohydrates.

38.  All cells utilize glucose to produce energy in form
of ATP via glycolysis or citric acid cycle
 Liver can also utilize the phosphogluconate
pathway which not only provides energy but also
produces an imp. Cofactor in the synthesis of
fatty acids.
 Most of glucose absorbed from meal is stored as
Glycogen in liver.
 When glycogen storage is exceeded in liver,
glucose is stored as fat.

39.  Only liver and muscle can store significant amount
of glycogen.
 Liver and kidney are unique in their capacity to
form lactate, pyruvate, amino acids & glycerol.
 Hepatic gluconeogenesis is vital in the
maintainence of a normal blood glucose
concentration.
 Glucocorticoids, catecholamines, glucagon &
thyroid hormone greatly enhance gluconeogenesis
– whereas insulin inhibits it.

40.  When carbohydrate stores are saturated liver converts the
excess ingested carbohydrates into fat.
 Fatty acids thus formed can be used immediately and stored
in adipose tissue or the liver for later consumption.
 Only RBCs and renal medulla can utilize only glucose.
 Neurons normally utilize only glucose but after a few days of
starvation they can switch to breakdown products of fatty
acids that have been made by liver as an energy source.

41. Liver performs an important function in protein
metabolism
Steps include-
1. Deamination from amino acids
2. Formation of urea
3. Interconversion between non essential amino
acids
4. Formation of plasma proteins

42.  Necessary for conversion of excess amino acids to
carbohydrates & fats
 Enzymatic processed convert amino acids to their
respective keto acids & produce ammonia.
 Deamination of alanine plays an important role in
hepatic gluconeogenesis.
 Liver normally deaminates most of amino acids
derived from dietary proteins
 Branched chain amino acids are primarily
metabolised by skeletal muscle.

43.  Ammonia formed from deamination is highly
toxic to tissue
 2 molecules of ammonia + CO2 – Urea
 Urea thus formed readily diffuses out of liver and
can be excreted by kidneys

44.  Hepatic transamination of appropriate keto acid
allows formation of non essential amino acids &
compensates for any dietary deficiency in these
amino acids

45. Nearly all plasma proteins with notable exceptions
of Ig are formed by liver.
 Quantitatively the most important of these proteins
are albumin, α1 – antitrypsin & other
proteases/elastases
Proteins produced by liver
 Albumin – maintains normal plasma oncotic
pressure and is principal binding & transport
protein for fatty acids & large no of hormones &
drugs.

46.  All coagulation factors which exception of
factor VIII & vonWille Brand factor are
produced in liver.
 Vit K is necessary co factor in synthesis of
Prothrombin, factor VII, IX & X
 Liver also produces plasma cholinesterase, an
enzyme that hydrolyses esters, including Local
anesthetics & Sch

47.  Protease inhibitors (antithrombin III, α1 –
antitrypsin)
 Transport proteins (Transferrin, Haptoglobin,
Ceruloplasmin)
 Complement
 α1 – acid glycoprotein
 C – reactive Protein
 Serum Amyloid - A

48.  It is divided into
1. Phase I reaction.
2. Phase II reaction.
3. Phase III reaction.

49.  It is oxidative hydrolysis & reduction reactions
 It is mainly microsomal oxidases, CYP isozymes
super family.
 These CYP isozymes are concentrated in the
centrilobular zone.
 It needs NADPH for its reactions and hence
formation of superoxides and reactive free
radicals, more chance of injury to these
cells, necrosis.

50.  Grapefruit juice.
 erythromycin,
 isoniazid,
 sulfonamides,
 ketoconazole

51.  Conjugation with the endogenous hydrophilic
molecules.
 It involves several processes such as
glucuronidation, sulphation, methylation, acetylation
.
 Glucuronidation is the common type.
 Hepatic microsomal uridine diphosphate glucuronyl
transferase mediates the reaction.

52.  These are susceptible to enzyme induction.
 Heavy smoking, phenytoin admistration seen to
increase glucuronidation in humans.
 In some drugs the conjugation ends up with a
metabolite more potent than the parent drug. Eg:
morphine- becomes morpine 6- glucuronide a potent
byproduct which is responsible for some of the
analgesia produced by morphine.

53.  It is a energy mediated transport/ elimination by
ATP- binding cassette transport proteins.
 Facilitates excretion of xenobiotics and endogenous
compounds.
 These proteins use ATP hydrolysis to drive
molecular transport.
 These resides on the canalicular surfaces of
hepatocytes and enables biliary excretion of cationic
compounds, including anticancer drugs.

54. • Genetic factors
• Diet
• Environment
• Age
• Enzyme Induction/Inhibition
• Liver disease
• Cardiac disease

55.  Factors : rate of hepatic blood flow, protein binding,
hepatic intrinsic clearance.
 Drug elimination – is volume of blood from which the
drug is completely removed per unit of time.
 Is equal to the product of hepatic blood flow and the
extraction ratio.
 Extraction ratio(E): amt of drug removed from the
blood during a simple pass through the liver.

56.  Anesthetics significantly alter extraction by
reducing hepatic blood flow.
 Inhalational agents may influence drug clearance
by altering drug-metabolizing ability or intrinsic
clearance
 Inhalational agents have been shown both in vitro
and in vivo to alter drug metabolism at clinically
relevant concentrations.
 They are competitively inhibiting p-450, and phase
II reactions.

57. High hepatic extraction
ratio
Low hepatic extraction
ratio
Lignocaine Diazepam
Propranolol Thiopentone
Meperidine Theophylline
Verapamil Digitoxin
Phenytoin
Pancuronium

58.  Liver plays an important role in hormone, vitamin &
mineral metabolism
 Normal thyroid function is dependent on hepatic
formation of the more active T3 from T4
 Liver is also mojor site of degradation for insulin,
steroid hormones, glucagon & ADH
 Hepatocytes are principal storage sites for Vit A, B12,
E, D & K.
 Hepatic production of transferrin & Haptoglobin is
important because proteins are important in iron
hemostasis.

59.  Hepatocytes make most of the pro-coagulants
with exceptions of Factors III, IV, VIII.
 Liver also makes protein regulators of
coagulation & the fibrinolytic pathways.
 Such regulators include protein
C, S, Z, Plasminogen Activator Inhibitor, &
antithrombin III

60.  Main site.
 Hemoglobin is heme and globulin, with heme
containing ferrous and porphyrin IX.
 20% approx, heme synthesised in the liver.
 Rate limiting step is synthesis of 5-
aminolevulinic acid catalysed by ALA
synthetase.

61.  Source is from the Heme metabolism.
 Approx 300mg of bilirubin formed everyday.
 80% by the phagosytosis of scenecent RBCs by the RE
cells.
 The extracted heme is converted to bilirubin, this is the
rate limiting step.
 This is then bound to albumin and liver processes the
molecules into conjugated bilirubin in 2 steps, and then
excreted.
 Enterohepatic circulation ensures some of these
products to return to the liver.

62. FUNCTIONS OF THE LIVER:
 Carbohydrate metabolism
Glycogenesis
Glycogenolysis
Gluconeogenesis
 Fat metabolism -
ketogenesis
 Protein metabolism
anabolism
deamination
urea formation
 Secretion of bile
 Detoxification
 Metabolism of
vitamins A,D,K,E &
 Clotting factors,
esp prothrombin
 Storage
 Blood store

63.  Anesthesia & anaesthetic drugs affects the
hepatic function by following mechanisms :
 Alteration in the hepatic blood flow n HABR.
 Metabolic function.
 Drug metabolism.
 Billiary function.

64. Effect of volatile agents on hepatic
blood flow :
Halothane: Causes hepatic arterial constincton,
microvascular vasoconstriction
Enflurane: Increase in hepatic vascular resistance
Isoflurane: Increase in microvascular blood velocity
Sevoflurane & Desflurane: Preservation of hepatic
blood flow & function

65.  KETAMINE: Little effect on hepatic blood flow
 PROPOFOL: Significant splanchnic vasodilator
increases both hepatic arterial & portal venous
blood flow
 THIOPENTONE & ETOMIDATE: Hepatic
arterial blood flow reduction, reducedf cardiac
output

66.  Vecuronium, rocuronium, mivacur
ium:
• Reduced elimination and Prolong duration of
action specially with infusion & repeated doses
 Atracurium & cisatracrium:
• Nondependant of hepatic metabolism and can
be used without modification of doses in end
stage liver disease

67.  Reduction in hepatic blood flow in high spinal &
epidural anesthesia
 Secondary to hypotension
 Reversed by vasopressors like dopamine,
ephedrine

68.  It is immunologically mediated, as it induces both
neoantigens & auto antigens. The incidence of fulminant
hepatic necrosis terminating in death associated with
halothane was found to be 1 per 35,000.
 Demographic factors ; It’s a idiosyncratic reaction,
susceptible population include Mexican Americans
,Obese women, , Age >50 yrs, , Familial predisposition,
Severe hepatic dysfunction while Children are resistant.
 Prior exposure to halothane is a important risk factor &
multiple exposure increases the chance of hepatitis.

69. ISOFLURANE- Isoflurane metabolism yields highly reactive
intermediates (TF-acetyl chloride; acyl ester) that bind covalently
to hepatic proteins. For this isoflurane most likely causes
hepatitis.
It undergoes minimal biodegradation, preserves microvascular
blood flow & oxygen delivery more than halothane or enflurane .
DESFLURANE- it is similarly biotransformed to trifluoroacyl
metabolites, appears even less likely than isoflurane to cause
immune injury because only 0.02 to 0.2% of this agent is
metabolized (1/1,000th that of halothane). Desflurane metabolites
are usually undetectable in plasma, except after prolonged
administration.

70. Desflurane ↓hepatic blood flow ,it markedly reduce oxygen
delivery to the liver and small intestine without producing
comparable reductions of hepatic oxygen uptake or hepatic and
mesenteric metabolism. Therefore, desflurane anesthesia may
decrease the oxygen reserve capacity of both the liver and the
small intestine.
SEVOFLURANE - It is metabolized more extensively than
isoflurane or desflurane,but slightly less than enflurane, and much
less than halothane.
The metabolism of sevoflurane is rapid (1.5 to 2 times faster than
enflurane), and produces detectable plasma concentrations of
fluoride and hexafluoroisopropanol (HFIP) within minutes of
initiating the anesthesia.
The liver conjugates most of the HFIP with glucuronic acid, which
is then excreted by the kidney.

71. NITROUS OXIDE-
it produces a mild increase in sympathetic nervous
system tone leads to mild vasoconstriction of the
splanchnic vasculature, leading to a decrease in portal
blood flow, and mild vasoconstriction of the hepatic
arterial system.
N2O is a known inhibitor of the enzyme methionine
synthase, which could potentially produce toxic
hepatic effects.

72.  Etomidate and thiopental at larger doses (>750 mg)
may cause hepatic dysfunction by ↓ hepatic blood
flow, either from ↑ hepatic arterial vascular resistance
or from reduced cardiac output and blood pressure.
 Ketamine has little impact on hepatic blood
flow, even with large doses
 Propofol increases Blood Flow in both the hepatic
arterial and portal venous circulation, suggesting a
significant splanchnic vasodilator effect

73.  Opioids have little effect on hepatic function, provided they
do not impair hepatic blood flow and oxygen supply. All
opioids increase tone of the common bile duct and the
sphincter of Oddi, as well as the frequency of phasic
contractions, leading to increases in biliary tract pressure
and biliary spasm.
 Morphine undergoes conjugation with glucoronic acid at
hepatic & extra hepatic site (kidney). The significantly
reduced metabolism of morphine in patients with
advanced cirrhosis leads to a prolonged elimination half-
life, markedly increased bioavailability of orally
administered morphine, decreased plasma protein
binding, and potentially exaggerated sedative and
respiratory-depressant effects. The oral dose of the drug
should be reduced because of increased bioavailability

74.  The volume of distribution of muscle relaxants,
may increase due to ↓ albumin an increase in γ-
globulin or the presence of edema.so the initial
dose requirements of these medications are
increased in cirrhotic patients and subsequent
dose requirements may be ↓, and drug effects
prolonged, owing to ↓ in hepatic blood flow and
impaired hepatic clearance, and possible
concurrent renal dysfunction.

75.  Vecuronium-it is a steroidal muscle relaxant It
undergoes hepatic elimination by acetylation.
Decreased clearance, a prolonged elimination half-
life, and prolonged neuromuscular blockade in
patients with cirrhosis .
 Rocuronium- another steroidal muscle relaxant
with a faster onset of action than vecuronium, also
undergoes hepatic metabolism and elimination.
Hepatic dysfunction can increase the volume of
distribution of rocuronium, thereby prolonging its
elimination half-life and producing a longer clinical
recovery profile and return of normal twitch tension.

76.  Atracurium & Cisatracurium
• Elimination half-lives and clinical durations of action
are similar in cirrhotic.82%to Bound albumin they
undergo clearance by organ-independent elimination
i.e. spontaneous non-enzymatic degradation
(Hoffmann's elimination).
• Laudanosine, a metabolite of both atracurium and
cisatracurium, is eliminated primarily by the liver; and
although its concentration may increase in patients
undergoing liver transplantation, clinically relevant
neurotoxicity has not been reported

77.  Altered protein binding
 Altered volume of distribution
 Altered drug metabolism due to hepatocyte
dysfuction

78.  Opioids: exaggerated sedative & respiratory
depressant effect and Half life is almost doubled
 Benzodiazepines : Duration of action increased
 Thiopentone, Etomidate, Propofol, Ketamine:
Repeated doses & prolong infusion causes
accumulation of drugs
 Increases risk of hepatic encephalopathy

79.  Splanchnic traction and exploratory laparotomy
can reduce blood flow to the intestines and the
liver
 Upper abdominal surgery is associated with the
greatest reduction in hepatic blood flow
 Elevation of liver chemistry tests is more likely
to occur after biliary tract procedures than after
nonabdominal procedures

80.  Liver major organ of metabolism
 Live dysfuction affects pharmacokinetics of
anesthetic drugs
 Anesthetic drugs affects liver function
 Neuroaxial blocks: reduction in hepatic blood flow
due to hypotension
 Intropetative
hypotension, hypoxia, hypocapnia, use of
hepatotoxic drugs in perioperative period can cause
postoperative hepatic dysfunction

81.  No one test reflects overall hepatic
function.
 Each test generally reflects one aspect of
hepatic function and must be interpreted
in conjunction with other tests alone with
clinical assessment of patient.
 Liver abnormalities can be divided into
1. Obstructive – affect biliary excretion of
substances
2. Parenchymal – result in generalised
hepatocellular dysfunction

82.  Normal total bilirubin - <1.5mg/dl
 Reflects balance between production &
biliary excretion.
 Jaundice is usually clinically obvious
when total bilirubin exceeds 2mg/dl
 >50% conj. Hyperbilirubinemia is ass. with
urinary urobilinogen & may reflect
hepatocellular dysfunction, intrahep.
Cholestasis or extrahepatic biliary
obstruction.
 >50% unconj. Hyperbilirubinemia may be
seen with hemolysis or cong. Or acquired
defects in bilirubin conjugation

83.  These enzymes are released into circulation
as a result of hepatocellular injury or death.
 AST is present in many tissues – liver, heart,
skeletal, muscle & kidneys.
 ALT is primarily located in liver & more
specific for hepatic dysfunction
 Normal – 35 to 45U/L
 Mild elevation can be seen in cholestasis or
metastatic liver disease.
 Abs. levels correlate poorly with degree of
hepatic injury in chronic conditions, but are
of great importance in acute liver disease. Eg-
drug overdose, ischaemic injury and
fulminant hepatitis.

84.  Is produced by liver, bone, small bowel,
kidneys & placenta.
 Excreted into bile
 Normal level – 25 to 85IU/L
 Most of circulating enzymes are derived from
bone.
 Biliary Obstruction – more hepatic alkaline
phosphatase is synthesized and released into
circulation.
 Increased levels indicate intrahepatic
cholestasis & biliary obstruction.
 Increased levels in pregnancy & Paget’s
disease

85. SGOT/SGPT BILIRUBIN ALKPO4
BILIARY OBS + ++ +++
HEPATITIS +++ + +
ALCOHOL/DRUGS N/+ ++ N

86.  Normal level – 3.5 to 5.5g/dl
 Albumin level may be normal with Acute
Liver Disease
 Albumin values <2.5g/dl are generally
indicative of CLD, acute stress or severe
malnutrition.
 Increased losses of albumin in urine is
suggestive of Nephrotic syndrome.

87.  Significant increase of blood ammonia
levels usually reflect disruption of hepatic
urea synthesis.
 Normal whole blood ammonia levels are 47
to 65mmol/L
 Increase usually reflect severe
hepatocellular damage.

88.  Normal level is 11 to 14secs. (Measures the
activity of fibrinogen & factors V, VII & X)
 Relatively short half time of factor VII (4 to
6Hrs)make PT useful in evaluating hepatic
synthesis function of pt with ALD or CLD.
 Prologation of PT >3 to 4s from control are
considered significant.
 Only 20 to 30% of normal factor activity is
required for normal coagulation, prolongation
of PT reflects severe liver disease unless Vit K
deficiency is +
 Failure of PT to correct following parenteral
administration of Vit K implies severe liver
disease

89.  Elevated serum LDH levels -
hepatocellular injury, extrahepatic
disorders or both.
 Extreme increases – massive liver damage
– fulm. Viral hepatitis, drug induced
failure or hypoxic hepatitis.
 Prolonged concurrent elevation –
malignant infiltration of liver.
 Notable hep disorders – hemolysis,
rhabdolysis, tumor necrosis, renal
infarction, acute CVA or MI. (severe
ecclampsia)

90.  Targeted testing is used to identify specific
hepatic or biliary diseases.
 Examples include –
1. Serologic testing to identify viral, microbial
& autoimmune causes.
2. Genetic testing to diagnose heritable
metabolic disorders.
3. Tumor marker assays to detect hepatic
malignancies

91.  Identifying viral markers – antibodies,
antigens and genetic material – is the key
for diagnosis of hepatitis from hepatotropic
viruses (A, B, C, E) and herpesviruses
such as CMV & EBV.
 Special tests – serum α1 – AT and
phenotype analysis.
 Markers for hepatic malignancy – AFP, des
– γ – carboxylated prothrombin.

92.  CBC- Hb may show anemia esp with the target
cells in jaundiced patients due to macrocytosis.
 Leucopenia- complicates portal HTN and
hypersplenism.
 Leucocytosis- in hepatic abscess, alcoholic
hepatitis, cholangitis.
 Thrombocytopenia- in cirrhosis, due to dec in
thrombopoetin in liver, and hypersplenism.

95.  Child-Pugh Score
 Model of End-Stage Liver Disease
Score(MELD)

96.  Child-Turcotte-Pugh (CTP) score
 initially designed to stratify the risk of portacaval shunt
surgery in cirrhotic patients
 based upon five parameters: serum bilirubin, serum
albumin, prothrombin time, ascites and
encephalopathy
 good predictor of outcome in patients with
complications of portal hypertension

97.  M&M for pts undergoing intra-abd
surgery
 Incorporates three
biochemical(PT, albumin, bilirubin)
 Incorporates three clinical
features(Nutrition, +/-
ascites, encephalopathy

99. Points Assigned 1 2 3
Laboratory value
Bilirubin (mg/adL) < 2 2-3 > 3
Albumin (g/dL) > 3.5 2.8-3.5 < 2.8
PT or
INR
< 4 s
< 1.7
4-6 s
1.7-2.2
> 6 s
> 2.2
Signs
Ascites None Slight Moderate
Encephalopathy None Stages 1-2 Stages 3-4
Child class A = 5-6 points; Child class B = 7-9 points; Child class C = 10-15 points
Child CG, Turcotte JG. Surgery and portal hypertension. In: The
Liver and Portal Hypertension. Child CG, ed. Philadelphia:
Saunders; 1964:50-64. Pugh RNH, et al. Br J Surg. 1973;60:648-652.

100.  Created in 1999 to predict 3 month
mortality in pts with chronic dz.
 Prioritizes those on transplat list
 Looks at bilirubin,INR,and serum
creatinine

102.  >8: predictive of poor
 >24: qualifies for transplantation