good

2.  The liver is a vital organ located in the upper
right quadrant of the abdomen, below the diaphragm. The
liver is a gland and plays a major role in metabolism with
numerous functions in the human body, including regulation
of glycogen storage, decomposition of red blood
cells, plasma protein synthesis, hormone production, and
detoxification.
 The liver plays a major role in carbohydrate, protein, amino
acid, and lipid metabolism.

:
carbohydrate metabolism
The liver performs several roles in
The liver synthesizes and stores approximately 100g
, the formation of glycogen
glycogenesis
via
glycogen
of
from glucose. When needed, the liver releases glucose into
, the breakdown
glycogenolysis
the blood by performing
The liver is also responsible
.
glucose
into
glycogen
of
from
glucose
, which is the synthesis of
gluconeogenesis
for
. Adipose and liver
glycerol
or
lactate
,
amino acids
certain
, which the liver
breakdown of fat
cells produce glycerol by
uses for gluconeogenesis.

3.  The liver plays a key role in digestion, as it produces
and excretes bile (a yellowish liquid) required for
emulsifying fats and help the absorption of vitamin K
from the diet. Some of the bile drains directly into
the duodenum, and some is stored in
the gallbladder.
 The liver is responsible for the breakdown and
excretion of many waste products. It plays a key role
in breaking down or modifying toxic substances
(e.g., methylation) and most medicinal products in a
process called drug metabolism. This sometimes
results in toxication, when the metabolite is more
toxic than its precursor. Preferably, the toxins
are conjugated to avail excretion in bile or urine. The
liver stores a multitude of substances, including
glucose (in the form of glycogen), vitamin A, vitamin
D , vitamin B12 ,vitamin K, iron, and copper. The liver
synthesizes angiotensinogen, a hormone that is
responsible for raising the blood pressure when
activated by renin, an enzyme that is released when
the kidney senses low blood pressure.

4.  LIVER DISEASE AND COAGULATION OUTCOMES:
 The liver plays a central role in the clotting process.
Acute and chronic liver diseases are invariably
associated with coagulation disorders due to
multiple causes including: decreased synthesis of
clotting and inhibitor factors, decreased clearance
of activated factors, quantitative and qualitative
platelet defects, hyperfibrinolysis, and accelerated
intravascular coagulation. The liver is the site of
production of most coagulation factors, but the
response of each factor to liver disease is variable
due to differences in biologic half lives and acute
phase reactions. The PT is usually prolonged first, then
APTT. Factor VII: shortest biologic half life, often
affected earliest with largest decrease in plasma
level. Factor VII also decreases earliest with warfarin
treatment. Factor VIII: may be normal or elevated
due to acute phase reactants. Factors XI and XII
:have long biologic half lives, and may be normal
until liver disease is advanced.

5. 
The liver plays a role in the production of
clotting factors as well as red blood cell
production. Some of the proteins synthesized
coagulation
by the liver include
XI
and
X
,
IX
,
VIII
,
VII
,
V
),
prothrombin
(
II
factors
protein
,
C
protein
, as well as
,
fetus
. In the first trimester
antithrombin
and
S
red blood
the liver is the main site of
nd week
32
production. By the
cell
has almost
bone marrow
, the
gestation
of
completely taken over that task. The liver is a
,
thrombopoietin
major site of production for
hormone that regulates the
glycoprotein
a
.
bone marrow
by the
platelets
production of

6.  As a result the PT, APTT, and all factors are
prolonged with the possible exception of
fibrinogen (I) and Factor VIII which . The bleeding
tendency accounts for increased risk of
morbidity and mortality in patients with liver
disease undergoing diagnostic or therapeutic
invasive procedures.
 Liver disease can cause both quantitative and
qualitative abnormalities in clotting
factors. Vitamin K-dependent factors (II, VII, IX
and X, Protein S, C and Z) undergo
posttranslational gamma-carboxylation, which
can be impaired by a deficiency of vitamin K or
by lack of blood-clotting enzymes in
hepatocellular disease. The presence and level
of vitamin K-dependent clotting factors that
have undergone incomplete or slight
carboxylation are also increased.

7.  The prothrombin time (PT) — along with its derived measures
of prothrombin ratio (PR) and international normalized
ratio (INR) — are assays evaluating the extrinsic
pathway of coagulation. This test is also called "ProTime INR"
and "PT/INR". They are used to determine the clotting
tendency of blood, in the measure of warfarin dosage, liver
damage, and vitamin K status. PT measures factors I
(fibrinogen), II (prothrombin), V, VII, and X. It is used in
conjunction with the activated partial thromboplastin
time (aPTT) which measures the intrinsic pathway and
common pathway.


The reference range for prothrombin time depends on the
analytical method used, but is usually around 12–13
seconds (results should always be interpreted using the
reference range from the laboratory that performed the
test), and the INR in absence of anticoagulation therapy
is 0.8-1.2. The target range for INR in anticoagulant use
. In some cases, if more intense
3
to
2
) is
warfarin
(e.g.
anticoagulation is thought to be required, the target range
may be as high as 2.5-3.5 depending on the indication for
anticoagulation.

8.  The partial thromboplastin time (PTT) or activated
partial thromboplastin time (aPTT or APTT) is a
medical test that characterizes blood coagulation.
Apart from detecting abnormalities in blood
clotting, it is also used to monitor the treatment
effects with heparin, a major anticoagulant. PTT is a
performance indicator of the efficacy of both the
"intrinsic" (now referred to as the contact activation
pathway) and the common coagulation pathways.
It is used in conjunction with the prothrombin
time (PT) which measures the extrinsic pathway.
 The typical reference range is between
30 seconds and 50 s (depending on laboratory).
Shortening of the PTT is considered to have little
clinical relevance, but some research indicates that
it might increase risk of thromboembolism. Normal
PTT times require the presence of the following
coagulation factors: I, II, V, VIII, IX, X, XI, & XII.
Notably, deficiencies in factors VII or XIII will not be
detected with the PTT test.

9.  International normalized ratio

The result (in seconds) for a prothrombin time
performed on a normal individual will vary
according to the type of analytical system
employed. This is due to the variations
between different batches of manufacturer's
tissue factor used in the reagent to perform
the test. The INR was devised to standardize
the results. Each manufacturer assigns an ISI
value (International Sensitivity Index) for any
tissue factor they manufacture. The ISI value
indicates how a particular batch of tissue
factor compares to an international
reference tissue factor. The ISI is usually
between 1.0 and 2.0.

12. 
blood
is an increase in the
hypertension
Portal
within a system of veins called the portal
pressure
,
stomach
the
venous system. Veins coming from
merge into the
pancreas
, and
spleen
intestine,
portal vein, which then branches into smaller
. If the vessels
liver
vessels and travels through the
are blocked due to liver
liver
in the
cannot flow properly through
blood
damage,
the liver. As a result, high pressure in the portal
system develops. This increased pressure in the
portal vein may lead to the development of
large, swollen veins (varices) within
, stomach, rectum, or umbilical
esophagus
the
area (belly button). Varices can rupture and
bleed, resulting in potentially life-threatening
complications.

13. 
The most common cause of
of the
cirrhosis
is
hypertension
portal
is scarring which
Cirrhosis
liver.
accompanies the healing of liver injury
, alcohol, or other
hepatitis
caused by
less common causes of liver damage. In
cirrhosis, the scar tissue blocks the flow

through the liver.
blood
of

15.  The main symptoms and complications of
portal hypertension include:
 Gastrointestinal bleeding marked by black,
tarry stools or blood in the stools,
or vomiting of blood due to the spontaneous
rupture and hemorrhage from varices
 Ascites (an accumulation of fluid in
the abdomen)
 Encephalopathy or confusion and
forgetfulness caused by poor liver function
 Reduced levels of platelets, blood cells that
help form blood clots, or white blood cells, the
cells that fight infection

16. 
defined
condition
medical
a
is
Hepatitis
and
liver
the
of
inflammation
the
by
characterized by the presence
the
of
tissue
the
in
cells
inflammatory
of
organ. Hepatitis is acute when it lasts less
than six months and chronic when it
persists longer.

17.  Chronic Hepatitis
 Chronic infection (carrier state) is
characterized by the persistence of low levels
of virus in the liver and serum viral antigens
(HBsAg, HBeAg, and HCVAg) for longer than 6
months without signs of liver disease. Persons
with this condition potentially are infectious to
others. The carrier state may persist for
decades or cause liver disease by progressing
to chronic active hepatitis.
 Chronic active hepatitis is characterized by
active virus replication in the liver, HBsAg and
HBeAg or HCVAg in the serum, signs and
symptoms of chronic liver disease, persistent
hepatic cellular necrosis, and elevation of
liver enzymes for longer than 6 months.

18.  1-Viral hepatitis
 Viral hepatitis is a collective term describing
liver inflammation or hepatitis caused by a
group of several different viruses.

The clinical manifestations of the five forms of
viral hepatitis are quite similar, and the
diseases can be distinguished from each
other only by serologic assays. The five known
causes of acute hepatitis are hepatitis virus
types A (HAV), B (HBV), C (HCV), D or delta
(HDV), and E (HEV) . All except HBV are RNA
viruses. Hepatitis A and hepatitis E are forms of
infectious hepatitis; they are spread largely by
the fecal-oral route

19.  Hepatitis B, hepatitis C, and hepatitis D are
forms of serum hepatitis, are spread largely by
parenteral routes and less commonly by
intimate or sexual exposure
 Unlike HAV hepatitis, infections by HBV and
HCV are bloodborne and/or often persist for
years, resulting in ongoing (chronic) but
usually asymptomatic liver inflammation and,
in some cases, scarring (cirrhosis) that leads to
liver failure and/or liver cancer.

20.  2-Alcoholic hepatitis:
Excessive alcohol consumption is a significant
cause of hepatitis and liver damage (cirrhosis).
 3-Toxic and drug-induced hepatitis: A large
number of medications and other chemical
agents can cause hepatitis. In the United
States acetaminophen, antibiotics, and central
nervous system medications are among the most
common causes of drug-induced hepatitis.
 4-Autoimmune: Autoimmune hepatitis is a
chronic disease caused by an abnormal immune
response against liver cells. The disease is thought
to have a genetic predisposition as it is
associated with certain human leukocyte
antigens.

21.  5-Non-alcoholic fatty liver disease: Non-
alcoholic fatty liver disease (NAFLD) is the
occurrence of fatty liver in people who have little
or no history of alcohol use. In the early stage
there are usually no symptoms, as the disease
progresses symptoms typical of chronic hepatitis
may develop. NAFLD is associated
with metabolic syndrome, obesity, diabetes,
and hyperlipidemia.
 6-Ischemic hepatitis: Injury to liver cells due to
insufficient blood or oxygen results in ischemic
hepatitis (or liver shock). The condition is most
often associated with heart failure but can also
be caused by shock or sepsis.
 7-Giant cell hepatitis: Giant cell hepatitis is a rare
form of hepatitis that predominantly occurs
in newborns and children.

22.  Clinical Manifestations

 In a typical, clinically apparent course of
acute resolving viral hepatitis, the incubation
period ranges from 2 to 20 weeks, as
determined largely on the basis of the viral
etiologic agent and exposure dose.

After an incubation phase that varies with
the infecting virus, approximately 10% of
hepatitis A, 60% to 70% of hepatitis C, and 70%
to 90% of hepatitis B cases are asymptomatic.
When manifestations occur, the clinical
features of acute viral hepatitis are similar and
are discussed together.

23.  Patients classically exhibit three phases of acute illness:
 -----The prodromal (preicteric) phase usually precedes the
onset of jaundice by 1 or 2 weeks and consists of abdominal
pain, anorexia, intermittent nausea, vomiting, fatigue,
myalgia, malaise, and fever.

 -----The icteric phase is heralded by the onset of clinical
jaundice, manifested by a yellow-brown cast to the
conjunctivae, skin, oral mucosa, and urine. Many of the
nonspecific prodromal symptoms may subside, but
gastrointestinal manifestations (e.g., anorexia, nausea,
vomiting, right upper quadrant pain) may increase. .The
onset of production of dark urine marks the icteric phase of
illness, during which jaundice appears and symptoms of
fatigue and nausea worsen. Typically, acute viral hepatitis
rarely is diagnosed correctly before the onset of jaundice.
Physical examination usually shows jaundice and hepatic
tenderness. In more severe cases, hepatomegaly and
splenomegaly may be present. Serum bilirubin levels (total
and direct) rise, and aminotransferase levels generally are
higher than 10 times the upper limit of normal. The duration
of clinical illness is variable; it typically lasts 1 to 3 weeks.

24.  the convalescent or recovery (posticteric)
phase, symptoms disappear, but
hepatomegaly and abnormal liver function
values may persist for a variable period. This
phase can last for weeks or months, with
recovery times for hepatitis B and hepatitis C
generally longer. The usual sequence is
recovery (clinical and biochemical) within
approximately 4 months after the onset of
jaundice.

25.  HEPATITIS A
 Hepatitis A (formerly known as infectious hepatitis) is
an acute infectious disease of the liver caused by the hepatitis A
virus (HAV). The clinical course of typical acute hepatitis A begins
with an incubation period that usually is 15 to 45 days in duration
(mean, 25 days).

 Early symptoms of hepatitis A infection can be mistaken
for influenza, but some sufferers, especially children, exhibit no
symptoms at all.
 ----Signs and Symptoms :
 Fatigue
 Fever
 Nausea
 Appetite loss
 Jaundice, a yellowing of the skin or whites of the eyes due
to hyperbilirubinemia, Jaundice occurs in 70% of adults infected
with HAV but in smaller proportions of children.
 Bile is removed from blood stream and excreted in urine, giving it
a dark amber colour
 Diarrhea
 Light, or clay-coloured faeces

26.  Transmission:

and infections often occur in
oral route
–
fecal
The virus spreads by the
conditions of poor sanitation and overcrowding.

 Diagnosis
 The diagnosis of acute hepatitis A is made by detection of IgM anti-HAV
in the serum of a patient with the clinical and biochemical features of
acute hepatitis.

 Prevention
 A safe and effective HAV vaccine is available and recommended for all
children 1 year of age and older and for persons at increased risk for
acquiring hepatitis A, including travelers to endemic areas of the world,
and injection drug users.
 The vaccine protects against HAV in more than 95% of cases for longer
than 25 years. The vaccine is given by injection. An initial dose provides
protection starting two to four weeks after vaccination; the second
booster dose, given six to twelve months later.

 Treatment

No specific therapies have been shown to shorten or ameliorate the
course of illness in hepatitis A. An important element of management
should be prophylaxis for contacts.

27.  HEPATITIS B

 Hepatitis B is an infectious disease caused by
the hepatitis B virus (HBV) which affects the liver.
It can cause both acute and chronic infections.
 Transmission:

Transmission of hepatitis B virus results from
exposure to infectious blood or body fluids
containing blood. Possible forms of transmission
and
blood transfusions
,
sexual contact
include
-
re
transfusion with other human blood products,
and
use of contaminated needles
from mother to
vertical transmission
and
syringes,
child during childbirth.

28.  Clinical Manifestations
 The typical course of acute, self-limited
hepatitis B begins with an incubation period
of 30 to 150 days(mean, 75 days). During the
incubation period, HBsAg, HBeAg, and HBV
DNA become detectable in serum and rise
to high titers.

Acute infection with hepatitis B virus is
an
–
hepatitis
associated with acute viral
illness that begins with general ill-health, loss
of appetite, nausea, vomiting, body aches,
mild fever, and dark urine, and then
.
jaundice
progresses to development of

29.  Diagnosis

, for detection
assays
The tests, called
of hepatitis B virus infection
that detect
blood tests
or
serum
involve
either viral antigens (proteins produced by
produced by the
antibodies
the virus) or
host. The hepatitis B surface antigen (HBsAg)
is most frequently used to screen for the
presence of this infection. The infectious
virion contains an inner "core particle"
enclosing viral genome. The icosahedral
core particle is made of 180 or 240 copies of
core protein, alternatively known as hepatitis
B core antigen, or HBcAg.

30. 
The icosahedral core particle is made of 180
or 240 copies of core protein, alternatively
known as hepatitis B core antigen, or HBcAg.
During this 'window' in which the host remains
infected but is successfully clearing the
hepatitis
antibodies specific to the
IgM
virus,
B core antigen (anti-HBc IgM) may be the
only serological evidence of disease.
Therefore most hepatitis B diagnostic panels
contain HBsAg and total anti-HBc (both IgM
and IgG).

31.  Shortly after the appearance of the HBsAg,
another antigen called hepatitis B e antigen
(HBeAg) will appear. Traditionally, the
presence of HBeAg in a host's serum is
associated with much higher rates of viral
replication and enhanced infectivity. During
the natural course of an infection, the HBeAg
may be cleared, and antibodies to the 'e'
antigen (anti-HBe) will arise immediately
afterwards. This conversion is usually
associated with a dramatic decline in viral
replication.

32. 
If the host is able to clear the infection,
eventually the HBsAg will become
IgG
undetectable and will be followed by
antibodies to the hepatitis B surface antigen
and core antigen (anti-HBs and anti HBc
IgG). The time between the removal of the
HBsAg and the appearance of anti-HBs is
. A person negative
window period
called the
for HBsAg but positive for anti-HBs either has
cleared an infection or has been vaccinated
previously. Individuals who remain HBsAg
positive for at least six months are considered
to be hepatitis B carriers.

33.  Prevention
 Vaccination against HBV is recommended for all
newborns, children, and adolescents, as well as
adults at risk for acquiring HBV, including health care
and public safety workers with exposure to blood,
injection drug users.
 Two formulations of HBV vaccine are available; both
are made by recombinant techniques using cloned
HBV S gene .For adults, the recommended regimen
is three injections of 1.0 mL (20 μg of Energix-B ) or 10
μg of Recombivax HB given intramuscularly in the
deltoid muscle at 0, 1, and 6 months.

 Treatment
 The use of antiviral therapy for acute hepatitis B is
controversial. Regimens of interferon alfa and
lamivudine are established therapies for chronic
hepatitis B, but they have not been adequately
evaluated for acute infection.

34.  HEPATITIS C
 Hepatitis C is an infectious disease affecting primarily the liver,
caused by the hepatitis C virus (HCV). The infection is
often asymptomatic, but chronic infection can lead to scarring of
the liver and ultimately to cirrhosis, which is generally apparent
after many years. In some cases, those with cirrhosis will go on to
develop liver failure, liver cancer.
 Transmission
 The primary route of transmission in the developed
world is intravenous drug use (IDU), while in the developing
world the main methods are blood transfusions and unsafe
medical procedures.
 ----Intravenous drug use :IDU is a major risk factor for hepatitis C in
many parts of the world.
 ----Healthcare exposure: Blood transfusion, transfusion of blood
products, or organ transplants without HCV screening carry
significant risks of infection.
 -----Sexual intercourse: Whether hepatitis C can be transmitted
through sexual activity is controversial. While there is an
association between high-risk sexual activity and hepatitis C.
 ----Body modification Tattooing is associated with two to threefold
increased risk of hepatitis C.

35.  Clinical Manifestations
 The clinical course of acute hepatitis C begins
with an incubation period that ranges from 15 to
120 days (mean, 50 days). During the incubation
period, often within 1 to 2 weeks of exposure,
HCV RNA can be detected by sensitive assays
such as those based on reverse transcriptase–
polymerase chain reaction (PCR).
 Acute infection
 Hepatitis C infection causes acute symptoms in
15% of cases. Symptoms are generally mild and
vague, including a decreased appetite,
fatigue, nausea, muscle or joint pains, and
weight loss and rarely does acute liver
failure result. Most cases of acute infection are
not associated with jaundice.

36.  Chronic infection
 About 80% of those exposed to the virus develop a
chronic infection. This is defined as the presence of
detectable viral replication for at least six
months. Chronic infection after several years may
cause cirrhosis or liver cancer. Fatty changes to the
liver occur in about half of those infected and are
usually present before cirrhosis
develops. Worldwide hepatitis C is the cause of 27%
of cirrhosis cases and 25% of hepatocellular
carcinoma.
 Prevention
 At present, there are no means of prevention of
hepatitis C other than avoidance of high-risk
behaviors and appropriate use of standard
precautions.
 Treatment
 Therapy with interferon alfa and ribavirin has been
shown to be beneficial in chronic hepatitis C.

37.  HEPATITIS D

 Hepatitis D, also referred to as hepatitis D
virus (HDV) and classified as Hepatitis delta
virus. HDV is considered to be a subviral
satellite because it can propagate only in the
presence of the hepatitis B virus (HBV).
 Transmission
 The routes of transmission of hepatitis D are
similar to those for hepatitis B

38.  Clinical Manifestations
 Delta hepatitis occurs in two clinical patterns
termed coinfection and superinfection.
 Coinfection is the simultaneous infection of
a host by multiple pathogen species. In virology,
coinfection includes simultaneous infection of a
single cell by two or more virus particles. An
example is the coinfection of liver cells
with Hepatitis B virus and Hepatitis D virus.
 Superinfection is the process by which a cell that
has previously been infected by
one virus gets co-infected with a different strain
of the virus, or another virus, at a later point in
time.


39.  Diagnosis
 The diagnosis of acute delta coinfection can be made in a
patient with clinical features of acute hepatitis who has HBsAg,
anti-HDV, and IgM anti-HBc in serum. Acute delta superinfection
is the occurrence of acute HDV infection in a person with
chronic hepatitis B or the HBsAg carrier state. The diagnosis of
superinfection can be made in a patient with clinical features of
acute hepatitis who has HBsAg and anti-HDV but no IgM anti-
HBc in serum. Other tests that are helpful in making the diagnosis
of ongoing HDV infection are determinations of serum HDV RNA
(detectable by PCR assay) and HDV antigen.

 Prevention
 The vaccine for hepatitis B protects against hepatitis D virus
because of the latter's dependence on the presence of
hepatitis B virus for it to replicate.

 Treatment
 No specific therapies are available for acute delta hepatitis.
Lamivudine and other anti-HBV agents are ineffective against
HDV replication.


40.  HEPATITIS E
 Hepatitis E is responsible for epidemic and endemic forms of
non-A, non-B hepatitis that occur in less developed areas of
the world.

 Clinical Manifestations
 TYhe clinical course of hepatitis E resembles that of other
forms of hepatitis. The incubation period is 15 to 60 days
(mean, 35 days). The disease frequently is cholestatic, with
prominence of bilirubin and alkaline phosphatase
elevations. Hepatitis E also tends to be more severe than
other forms of epidemic jaundice, with a fatality rate of 1%
to 2% and a particularly high rate of acute liver failure in
pregnant women. HEV virions and antigen can be
detected in stool and liver during the incubation period and
early symptomatic phase, but these tests are not practical
methods of diagnosis. ELISAs for IgM and IgG antibody to
HEV (anti-HEV) have been developed .
 Prevention and Treatment
 There are no known means of prevention or treatment of
hepatitis E.

41.  Dental Management

 1-The identification of potential or actual
carriers of HBV, HCV, and HDV is
problematic, because in most instances
carriers cannot be identified by history.
Therefore, all patients with a history of
viral hepatitis must be managed as
though they were potentially infectious.


42. 
2-The recommendations for infection control
practice in dentistry published by the CDC
and the American Dental Association have
become the standard of care to prevent
cross-infection in dental practice ( Appendix
B). These organizations strongly recommend
that all dental health care workers who
provide patient care receive vaccination
against hepatitis B virus and implement
standard precautions during the care of all
dental patients.

43. 
3-Patients with Active Hepatitis. No dental
treatment other than urgent care (absolutely
necessary work) should be rendered for a
patient with active hepatitis unless the patient
has attained clinical and biochemical
recovery . Urgent care should be provided
only in an isolated operatory with strict
adherence to standard precautions . If
surgery is necessary, a preoperative
prothrombin time and bleeding time should
be obtained and abnormal results discussed
with the physician. The dentist should refer the
patient who has acute hepatitis for medical
diagnosis and treatment.

44.  4-Patients with a History of Hepatitis. Most carriers
of HBV, HCV, and HDV are unaware that they
have had hepatitis. An explanation is that many
cases of hepatitis B and hepatitis C apparently
are mild, subclinical, and nonicteric. such cases
may be essentially asymptomatic or resemble a
mild viral disease and therefore go undetected.
 Thus, the only practical method of protection
from exposure to potential infection associated
with providing dental care for persons with
undiagnosed hepatitis, or with other undetected
infectious diseases, is to adopt a strict program of
clinical asepsis for all patients . In addition, use of
the hepatitis B vaccine further decreases the
threat of hepatitis B infection.

45.  For those patients who provide a positive
history of hepatitis, additional historical
information occasionally can be of some help
in determining the type of disease.
 An additional aspect of a prudent approach
to provision of clinical care for patients with a
history of hepatitis of unknown type is to use
the clinical laboratory to screen for the
presence of HBsAg or anti-HCV. Such
screeening may be indicated even in persons
who specifically indicate which type of
hepatitis they had, because information
provided in patient histories of this type is
unreliable 50% of the time..

46. 
5- Patients at High Risk for HBV or HCV Infection.
Several groups are at unusually high risk for HBV
and HCV infection . Screening for HBsAg and
anti- HCV is recommended in persons who fit into
one or more of these categories unless they are
already known to be seropositive. If a patient is
found to be a carrier, this knowledge could be of
extreme importance for the modification of
lifestyle. In addition, the patient might have
undetected chronic active hepatitis, which
could lead to bleeding complications or drug
metabolism problems. Finally, if an accidental
needle stick or puncture wound occurs during
treatment and the dentist is not vaccinated (or
antibody titer status is unknown), knowing
whether the patient was HBsAg- or HCV-positive
would be of extreme importance in determining
the need for HBIG, vaccination, and follow-up
medical care.

47.  6-Patients Who Are Hepatitis Carriers. If a
patient is found to be a hepatitis B carrier
(HBsAg-positive) or has a history of hepatitis C,
standard precautions must be followed to
prevent transmission of infection.
 In addition, some hepatitis carriers may have
chronic active hepatitis, leading to
compromised liver function and interference
with hemostasis and drug metabolism.
Physician consultation and laboratory
screening of liver function are advised to
determine current status and future risks.

48.  7- Nonsteroidal antiinflammatory drugs
(NSAIDs), including aspirin, and
acetaminophen, as well as codeine and
meperidine, should be avoided or their use
very limited in persons .

 8-Antibiotic prophylaxis is not recommended;
however, patients who have severe liver
disease may be more susceptible to infection.
Selection of antibiotic agent is based on risk
and severity of dental infection. Avoid use of
metronidazole and vancomycin .

49.  9-Higher doses may be required to achieve
adequate anesthesia in presence of alcoholic
liver disease. Knowledge of current liver function
is important to establish proper dosages.
Epinephrine (1 : 100,000, in a dose of no more
than two carpules) in local anesthetics generally
is not associated with any problems, but patients
should be monitored closely.
 10-Use anxiety/stress reduction techniques as
needed, but avoid benzodiazepines.

 11-Excessive bleeding may occur in the patient
with end-stage liver disease. Most such patients
will have reductions in coagulation factors and
thrombocytopenia, so they are at greater risk for
postsurgical bleeding; they may need vitamin K
and/or platelet or clotting factor replacement.


50.  12-Monitor blood pressure, because it may be
significantly increased with portal hypertension in
patients with end-stage liver disease.

 13-Because many medications are metabolized
in the liver, certain drugs may need to be
avoided or reduced in dosage. Limit or avoid use
of acetaminophen, aspirin, ibuprofen, codeine,
meperidine, diazepam, barbiturates,
metronidazole, and vancomycin. The use of
epinephrine or other pressor amines (in gingival
retraction cord or to control bleeding) must be
limited, especially if portal hypertension is
present.




51.  ALCOHOLIC LIVER DISEASE
 Definition
 The exact effect of alcohol on the liver was not known until researchers
demonstrated that alcohol is hepatotoxic and its metabolite,
acetylaldehyde, is fibrinogenic.

 Pathophysiology and Complications
 The pathologic effects of alcohol on the liver are expressed as one of
three disease entities. The earliest change seen in alcoholic liver disease
is so-called fatty liver, characterized by presence of a fatty infiltrate. The
hepatocytes become engorged with fatty lobules and distended, with
enlargement of the entire liver. No other structural changes usually are
noted. This condition may emerge after only moderate usage of alcohol
for a brief time; however, it is considered completely reversible.
 A second and more serious form of alcoholic liver disease is alcoholic
hepatitis. This diffuse inflammatory condition of the liver is characterized
by destructive cellular changes, some of which may be irreversible.
 Classically, severe alcoholic steatohepatitis (formerly called ―alcoholic
hepatitis‖) is characterized by the sudden development of tender
hepatomegaly, jaundice, and fever in an person who has been drinking
heavily. Often, the illness is associated with a flu-like prodrome that
includes malaise, anorexia, and weakness.

52.  The third and most serious form of
alcoholic liver disease is cirrhosis, which
generally is considered an irreversible
condition characterized by progressive
fibrosis and abnormal regeneration of
liver architecture in response to chronic
injury or insult (i.e., prolonged and heavy
use of ethanol) . Cirrhosis results in the
progressive deterioration of the
metabolic and excretory functions of the
liver, ultimately leading to hepatic
failure.

53. 
Hepatic failure is manifested by myriad of
health problems. Some of the more
important of these are esophagitis, gastritis,
and pancreatitis, which contribute to
generalized malnutrition, weight loss,
protein deficiency (including coagulation
factors), impairment of urea synthesis and
glucose metabolism, endocrine
disturbances, encephalopathy, renal
failure, portal hypertension, and jaundice.
Accompanying portal hypertension is the
development of ascites and esophageal
varices . In some patients with cirrhosis,
blood from bleeding ulcers and
esophageal varices is incompletely
metabolized to ammonia, which travels to
the brain and contributes to
encephalopathy.

54.  Bleeding tendencies are a significant feature in advanced
liver disease. The basis for the diathesis is in part a
deficiency of coagulation factors, especially the
prothrombin group (factors II, VII, IX, and X). These factors all
rely on vitamin K as a precursor for production . Vitamin K is
absorbed from the large intestine and stored in the liver,
where it is converted into an enzymatic cofactor for the
carboxylation of prothrombin complex proteins.
Widespread hepatocellular destruction as seen in cirrhosis
decreases the liver’s storage and capacity for conversion of
vitamin K, leading to deficiencies of the prothrombin-
dependent coagulation factors. In addition to these
deficiencies, thrombocytopenia may be caused by
hypersplenism secondary to portal hypertension and to
bone marrow depression. Anemia and leukopenia also may
result from toxic effects of alcohol on the bone marrow and
nutritional deficiencies. Accelerated fibrinolysis also is seen.


55.  Clinical Presentation
 Alcoholic cirrhosis may remain asymptomatic
for many years until sufficient destruction of the
liver parenchyma has occurred to produce
clinical evidence of hepatic failure. Ascites,
spider angiomas , ankle edema, and jaundice
may be the earliest manifestations, but
frequently hemorrhage from esophageal
varices
 is the initial sign. The hemorrhagic episode may
herald rapid progression to hepatic
encephalopathy, coma, and death. Other,
less specific signs of alcoholic liver disease
include anemia, purpura, ecchymoses,
gingival bleeding, palmar erythema, nail
changes, and parotid gland enlargement
(known as sialadenosis).


56.  Laboratory Findings
 Liver abnormalities cause elevations of bilirubin,
alkaline phosphatase, AST(aspartate amino
transfrase), ALT( alenine amino transfrase),
amylase, uric acid, triglyceride, and cholesterol
levels. Leukopenia (or leukocytosis) or anemia
often is present.

 Alcoholic liver disease also leads to
deficiencies of clotting factors reflected as
elevations in the prothrombin time and partial
thromboplastin time. Thrombocytopenia may
be present owing to hepatosplenomegaly,
causing a decreased platelet count. Increased
fibrinolytic activity may be evidenced by a
prolonged thrombin time or a decreased
euglobulin clot lysis time.

57.  Dental Management
 Treatment Considerations.
 1-For a patient with alcoholism are
recognized: (1) bleeding tendencies, (2)
unpredictable metabolism of certain drugs,
and (3) risk of spread of infection. A CBC
(complete blood count) with differential
and determinations of AST and ALT,
bleeding time, thrombin time, and
prothrombin time are sufficient to screen for
potential problems. Abnormal laboratory
values, on a background of suggestive
findings on the clinical examination or a
positive history, constitute the basis for
referral to a physician for definitive
diagnosis and treatment.

58.  2-A patient with untreated alcoholic liver disease is
not a candidate for elective, outpatient dental care
and should be referred to a physician. Once good
medical management has been instituted and the
patient appears stable, dental care may be
provided after consultation with the physician.

 3-In cases in which the patient has not been seen by
a physician within the past several months, screening
laboratory tests should be ordered, including CBC
with differential and determinations of AST and ALT,
platelet count, thrombin time, and prothrombin time,
before invasive procedures are undertaken.

 4-Bleeding diatheses should be managed in
conjunction with the physician and may entail use of
local hemostatic agents, fresh frozen plasma, vitamin
K, platelets, and antifibrinolytic agents.


59.  5-A second area of concern in patients with alcoholic liver
disease is the unpredictable metabolism of drugs. This
concern is two-fold: In mild to moderate alcoholic liver
disease, significant enzyme induction is likely to have
occurred, leading to an increased tolerance of local
anesthetics, sedative and hypnotic drugs, and general
anesthesia. Thus, larger-than-normal doses of these
medications may be required to obtain the desired effects.
 Also, with more advanced liver destruction, drug
metabolism may be markedly diminished, potentially
leading to an increased or unexpected effect. For
example, if acetaminophen is used in usual therapeutic
doses in chronic alcoholism, or if acetaminophen is taken
with alcohol during a fasting state, severe, fatal
hepatocellular disease may result. The dentist should
exercise caution in use of the drugs listed below when
treating patients with chronic alcoholism.


60.  Local Anesthetics*
 Lidocaine (Xylocaine)
 Mepivacaine (Carbocaine)
 Prilocaine (Citanest)
 Bupivacaine (Marcaine)
 Analgesics
 Aspirin†
 Acetaminophen (Tylenol, Datril)†
 Codeine‡
 Meperidine (Demerol)‡
 Ibuprofen (Motrin)†
 Sedatives
 Diazepam (Valium)‡
 Barbiturates‡
 Antibiotics
 Ampicillin
 Tetracycline
 Metronidazole§

Vancomycin§

61. 
6--A third area of concern is risk for infection
or spread of infection in the patient who
has alcoholic liver disease. Risk increases
with surgical procedures or trauma, which
can introduce oral microorganisms into the
blood circulation, with less efficient
elimination by the reticuloendothelial
system owing to impaired cellular function.
Although patients who have alcoholic liver
disease exhibit reduced reticuloendothelial
functional capacity and altered cell-
mediated immune function, studies do not
indicate that antibiotic prophylaxis should
be provided before invasive dental
procedures in the absence of an ongoing
infection.

62.  7-Liver enzyme induction and central
nervous system effects of alcohol in patients
with alcoholism can require use of
increased amounts of local anesthetic or
additional anxiolytic procedures.
Appointments with these patients may
therefore require more than the scheduled
time if this manifestation was not
anticipated.
 Alcohol has a deleterious effect on neural
development,the corticotropin-releasing
hormone system, metabolism of
neurotransmitters, and the function of
neurotransmitter receptors. As a result, the
acetylcholine and dopaminergic systems
are impaired, causing sensory and motor
disturbances (e.g., peripheral
neuropathies).

63.  Oral Complications and Manifestations

Poor hygiene and neglect (as evidenced by caries) are
prominent oral manifestations of chronic alcoholism. In
addition, a variety of other abnormalities may be found .
Patients with cirrhosis have been reported to have impaired
gustatory function and are malnourished. Nutritional
deficiencies can result in glossitis and loss of tongue
papillae, along with angular or labial cheilitis, which may be
complicated by concomitant candidal infection. Vitamin K
deficiency, disordered hemostasis, portal hypertension, and
splenomegaly (causing thrombocytopenia) can result in
spontaneous gingival bleeding and mucosal ecchymoses
and petechiae. In some instances, unexplained gingival
bleeding has been the initial complaint of alcoholic
patients. A bilateral, painless hypertrophy of the parotid
glands, termed sialadenosis, is a frequent finding in patients
with cirrhosis.

64. 
Alcohol abuse and tobacco use are strong
risk factors for the development of oral
squamous cell carcinoma, and as with all
patients, the dentist must be aggressive in
the detection of unexplained or suspicious
soft tissue lesions (especially leukoplakia,
erythroplakia, or ulceration) in chronic
alcoholics. Sites with a marked predilection
for development of oral squamous cell
carcinoma include the lateral border of the
tongue and the floor of the mouth.