A PowerPoint presentation on Liver Disease for dental residents.

1. Jeffery L. Hicks, D.D.S.
Dept. of Comprehensive Care Dentistry

2. Largest internal organ
Weight ~3 lbs
Upper Right Quadrant of
abdominal cavity
Beneath the diaphragm,
protected by rib cage

3. Four lobes
Hepatocytes / lobules
Lobule / central venule
Hepatic artery & portal vein
peripheral to each lobule
Sinusoids carry blood between
central venules and hepatic
artery / portal vein branches

4. Via hepatic artery / portal vein
Portal vein drains intestines,
stomach, spleen and
esophagus
Portal vein provides 60% of the
liver’s blood supply

5. Formation and excretion of bile
Regulation of carbohydrate homeostasis
Lipid synthesis and secretion of plasma lipoproteins
Control of cholesterol homeostasis
Formation of urea, serum albumin, clotting factors, enzymes
Detoxification of drugs and foreign substances

6. Inflammation of the liver
Hepatitis - viral, bacterial,
toxic, drug-induced or
idiopathic/cryptogenic
Hepatitis - acute or chronic
Hepatitis may lead to cirrhosis

7. Upon systemic entry, virus
infects hepatocytes
Viral antigens are displayed on
hepatocyte surfaces
Cytotoxic T-cells attack
antigens on hepatocytes
resulting in inflammation
and necrosis

8. Incubation phase: variable depending on virus
Symptomatic preicteric phase: malaise, fatigue, nausea, appetite loss
Symptomatic icteric phase: jaundice, light-colored stools, pruritis
Convalescence: clearance of jaundice and systemic symptoms

9. Hepatitis A virus (HAV) is a childhood disease
~ 50% of individuals in the US have been infected by adulthood
Associated with oral-fecal contamination (food, water)

10. Found in feces 2 or more weeks before onset of symptoms
Infectious until 2 weeks after symptoms begin
Presence of anti-HAV antibody in serum indicates prior sensitization
to HAV and can offer protection from future infection
99% of people infected with HAV clear infection without treatment

11. Hepatitis B is caused by DNA
viron with envelop
HBV components:
envelope contains HBsAg
(surface antigen)
HBcAG and HBeA
(core antigens)

12. HBV found in mult. body fluids
Transmission via body fluid
contact with a mucous
membrane, non-intact skin,
percutaneous exposure
HBV can survive on surfaces
for over one week
Highest concentration of HBV
particles are found in blood

14. No TX indicated for acute B
TX of chronic symptoms
associated with HBV
Interferon reduces liver
damage
in 30% symptomatic chronic
Adefovir (nucleotide analogs)
results in viral load reduction
Liver transplant if dz progress

15. Hepatitis C is caused by
enveloped RNA virus
Envelope protein rapid mutate
6 different genotypes with
50 subcategories with
variations - quasispecies

16. “Mild” type of acute HCV has
high rate of progression to
chronic dz and eventual
cirrhosis
Chronic Hepatitis C progresses
~10-30 yrs
Acute Hepatitis
Chronic Hepatitis
Fulminant Hepatitis
Cirrhosis
Cancer
Death
Subclinical Dz Symptomatic Dz

17. ELISA to detect HCV antibodies
RIBA as a confirmatory test
Hep C PCR with viral genotyping
LFT’s are performed to assay baseline liver enzyme which if
elevated may indicate hepatocyte damage

18. Genotypes 2 and 3 are more
likely to respond to
treatment
10
goal is to eradicate HCV
infection and reduce
incidence of hepatocellular
carcinoma
Interferon and ribavarin
therapy
Pegylated interferon
Liver transplant

19. HEV is an RNA virus with oral-fecal transmission
Also known as enteric non-A, non-B hepatitis
Occurs primarily in developing countries with poor sanitation
Epidemics have occurred in Mexico, India, Asia and Africa
Serologic test not available, diagnosis is one of exclusion
Incubation period is 15-64 days

20. Symptoms include nausea,
vomiting, abnormal LFT’s
Treatment is supportive
Liver transplant if necessary

21. Also referred to as cryptogenic or autoimmune hepatitis
LFT’s are elevated without evidence of viral antigens
70-80% of patients are female
Treated with corticosteroids and immunosuppressive agents
Methylprednisone-1st
line therapy as well as Imuran (Azathioprine)

22. Cirrhosis - chronic, progressive
Hepatocytes try to regenerate
growth is uncontrolled and
fibrous, leading to impeded
vascular flow

23. Most common type
1st change - accumulation of fat in the liver cells
Fatty liver is reversible if ETOH use is stopped
If not, widespread scar formation occurs throughout the liver

24. Chronic biliary obstruction or
infection
Diffuse fibrosis of the liver
with jaundice

25. Abrupt onset of GI disturbances such as flatulence, nausea and
vomiting, diarrhea or constipation due to altered liver
metabolism of carbs, fats and proteins
Dull heavy pain in the right upper quadrant
Liver and spleen enlargement with a palpable liver

26. Later manifestations due to
liver failure and
portal hypertension
Jaundice
Peripheral Edema
Ascites
Esophageal Varices
Skin Lesions
Hematologic Disturbances

27. Accumulation of fluid in the
abdominal cavity
Protein moves from liver
sinusoids into the lymph
space
lymph leaks through capsule
into the abdominal cavity
Paracentesis
Diuretics used to remove excess
fluid (lasix, HCTZ)

28. Accumulation of fluid may lead
to spontaneous bacterial
peritonitis (SBP)
Cipro prophylactically to
prevent (SBP)

29. Graded I – IV; occurs in
2/3 to ¾ of cirrhotic patients
Fibrosis causes portal vein
HTN; blood flow is impeded
collateral circ. develops

30. Veins of the esophagus thin,
not elastic, fragile, bleed
Varices rupture in response
GERD, ingestion of coarse,
poorly chewed food,
vomiting, straining at stool,
coughing, sneezing or lifting
heavy objects
Result- melena or hematemesis
Bleeding varicies the most life-
threatening medical
emergency

31. Collateral circulation of
abdominal veins due to
portal hypertension

32. Propranolol, nonselective beta blocker
Reduce hepatic blood flow by reducing cardiac output
Avoid epi use = unopposed alpha action = hypertensive crisis
Surgical shunting, namely TIPS (Transjugular Intrahepatic
Portosystemic Shunt)

33. TIPS: needle inserted into right
internal jugular vein,
advanced into a hepatic vein
and then into a large branch
of the portal vein,
this tract is widened with
balloon and a wire mesh
stent
is placed in the tract to
maintain patency.

34. Spider angiomas small dilated
blood vessels with a
bright red center point and
spider like branches
Occur on the nose, cheeks,
upper trunk, neck and
shoulders
Intraoral petechiae and
ecchymosis are also common

35. NH3 produced in gut by bacterial breakdown of amino acids,
amines, purines and urea.
NH3 shunted into systemic circulation and causes confusion,
mental status changes, deep coma and death
Managed via Lactulose, laxative that is converted to acetic acid
in the gut to decrease ph to discourage bacterial growth
Lactulose traps ammonia in the gut and the laxative effect
expels ammonia in the feces.

36. Asterixis (liver flap)
pt/ is unable to hold out arms
with hands dorsiflexed
Rapid flexion and extension
movements of hands occur

37. Liver panel
Serum bilirubin
ALP
GGT
AST
ALT
Serum albumin
PTT
INR (PT)
WBC
Platelet count

38. Consider antibiotic prophylaxis due to decrease of Kupffer cells
No official recommendation exists
Obtain recent WBC, platelet count and PTT, INR,
usually 1 month old labs may be suitable but
if patient has severe liver disease then more recent labs needed
due to unpredictability of values

39. When evaluating PTT, INR and platelet counts prior to Tx,
decision to render treatment is made on a case-by-case basis
Platelet transfusion and FFP necessary if platelets are 50K or less
and if INR is 2 or above and or if PTT is 2x normal value
Collaplug, Avitene, Topical Thrombin and primary closure
necessary
for low platelet counts and elevated coagulation tests

40. Pt. may breakthough bleed
due to clot breakdown/
fibrinolysis
Amicar mouthrinse to slow clot
breakdown
May need cryoprecipatate
Oral stents as carrier for agents
and apply pressure
10
Closure, always!

41. Analgesia - avoid all NSAIDS
renal toxicity,
hepatorenal syndrome
Acetaminophen acceptable at
doses < 4 gms daily
Pt’s physician should be
consulted for alternative
medications

42. Increase in transplant success
and survival rates:
anti-rejection medications
organ preservation solutions.
One-year patient survival rates
85% to 90%
Five-year patient survival rates
65%

43. Average OR time: 8-12 hours
Average hospital stay: 2 weeks
Average blood transfusion:
5 units

44. Following transplantation
patients are placed on
immunosuppressive drugs
In the OR with varying doses.
Adjusting doses avoids risk of
post-operative infection,
tumor development and
liver rejection.

45. Immunosuppressives
Corticosteroid, usually prednisone
fluid build-up and puffiness of the face
Cyclosporine (Neoral)
high blood pressure, kidney damage, growth of body hair
Tacrolimus (Prograf) (Tacrolimus)
lowest side effects
Frequent blood tests are required to monitor the patient's progress
and reduce side effects.

46. As time passes, the amount of
immunosuppression needed
usually decreases
Be aware if patients are taking
meds as indicated
Antibiotic prophylaxis is
required for life in all organ
transplant patients prior to
invasive dental procedures