1
Q
Liver
A
Largest internal organ; located in the R upper quadrant
2
Q
liver blood supply
A
➢ ~ 20 % Hepatic artery - oxygenated blood
➢ 80% Portal vein –nutrients
3
Q
bile duct system
A
Common Hepatic Duct
- left and right hepatic ducts forms the common hepatic duct
- drains bile from the liver
- transports waste from the liver and aids in digestion by releasing bile
Common Bile Duct
- carries bile from the liver and the gallbladder through the pancreas and into the duodenum
- part of the biliary duct system; formed where the ducts from the liver and gallbladder are joined
4
Q
Hepatic Veins
A
drain venous blood from liver to inferior vena cava and on to the right
5
Q
Hepatic Artery
A
Hepatic Artery – provides oxygen and nutrition to liver tissues
6
Q
Hepatic Portal Vein
A
delivers substances absorbed by the gastrointestinal tract (stomach, intestine, spleen and pancreas) for metabolic conversion and/or removal in the liver
7
Q
hepatocytes proteins produced
A
- Immunoglobulins
- Albumin
- coagulation factors
- carrier proteins
- growth factors
- hormones
8
Q
bilirubin
A
role of hepatocytes
➢ bilirubin is from breakdown of RBCs; bilirubin transported to liver by being bound to albumin (unconjugated form)
➢ Liver conjugates bilirubin by unbinding the protein binding it to glucose; this unconjugated form is in bile
➢ Produces bile for digestion
➢ Produces cholesterol for fat storage
9
Q
Bilirubin levels escalate from:
A
➢ Blood disorders - hemolytic anemia, sickle cell anemia, inadequate transfusions
➢ **Chronic liver disease **
➢ Blockage of bile ducts in liver or gallbladder
➢ Viral hepatitis, EtOH induced hepatitis; drug induced hepatitis, cirrhosis, etc.
➢ Increased bilirubin –jaundice, fatigue, cutaneous itch, discolored urine, discolored feces (?)
10
Q
nutritional function hepatocytes
A
➢ Regulates nutrients
- glucose
- glycogen
- lipids
- amino acids
11
Q
excretion function hepatocytes
A
➢ Prepares drugs for excretion
➢ Responsible for drug conjugation and metabolism
oBilirubin conjugation
oPhase I –cytochrome P450; can produce toxic metabolites
oPhase II –conjugation (glucuronidation, sulfation, inactivation by glutathione, etc.)
12
Q
forms of damage at liver
A
➢ Hepatocellular (inflammation and injury)
➢ Cholestatic (obstructive)
➢ Mixed
➢ Cirrhosis (fibrotic, end-stage); acute or chronic
➢ Neoplastic
13
Q
general signs of liver dx
➢ skin?
➢ gut?
➢ swelling?
➢ bleed?
➢ urine?
➢ stool?
➢ Mental?
➢ eyes?
➢ Spider angiomas
➢ Palmar erythema
➢ nn?
➢ skin?
A
➢ Jaundice
➢ Ascites
➢ Edema
➢ GI bleed
➢ Dark urine
➢ Light stool
➢ Mental confusion
➢ Xanthelasma
➢ Spider angiomas
➢ Palmar erythema
➢ Asterixis
➢ Hyperpigmentation
14
Q
symptoms liver dx
A
➢ Appetite loss ֎
➢ Bloating
➢ Nausea
➢ RUQ pain
➢ Fatigue
➢ Mental confusion
15
Q
Xanthelasma
A
fatty chol deposits in occular area
16
Q
spider angiomas
A
poor clotting factors= capillary fragibility
17
Q
Asterixis
A
- a.k.a. flapping tremor
- classic sign in hepatic encephalopathy (HE)
- jerky movements when hands are extended at wrists.
18
Q
hepatic encehpalopathy
A
19
Q
Asterixis pathogenesis
A
20
Q
common blood tests
A
*Complete Blood Count (CBC)
*Comprehensive Metabolic Panel (CMP)
*Multiple others available for specific patient evaluations
21
Q
Complete Blood Count (CBC)
A
- evaluate the cells that circulate in blood: red blood cells (RBCs), white blood cells (WBCs), platelets (PLTs)
- indicator of overall health
- may detect a variety of diseases and conditions
22
Q
Comprehensive Metabolic Panel (CMP)
A
- aka chemical screen or, SMAC 14 (Sequential Multiple Analysis –Computer)
- consists of 14 blood tests which serves as an initial broad medical screening tool
- Includes
- General tests
- Kidney function assessment
- Electrolytes
- Protein tests
- Liver function assessment
- there are also SMAC 8, 12, 16 and 20 variants
23
Q
Liver Function Tests
A
*Bilirubin
*Alkaline phosphatase (ALP)
*Transaminases
- Aspartate amino transferase (AST)
- Alanine amino transferase (ALT)
- Gama-Glutamyl Transferase (GGT)
*Albumin
*Globulin
24
Q
high bilirubin levels
A
oProduct of heme breakdown
oIncreased total bilirubin, increased severity of liver injury
measured in congugated and unconguated forms
25
uncongugated bilirubin
oUnconjugated (indirect)
❖Insoluble, bound to albumin, not filtered by kidney
❖Increased SERUM not really indicative of liver disease,
❖indicates hemolysis, ineffective erythropoiesis (thalassemia,
vitamin B deficiency, Gilbert syndrome)
26
congugated bilirubin
oConjugated bilirubin (direct)
❖Increased SERUM indicative of liver disease
❖Water-soluble, excreted by kidney
❖All URINE bilirubin is conjugated
27
➢ Alkaline phosphatase (high)
oaltered in myriad of diseases especially bone neoplasms
onot specific to liver disease,
omay indicate cholestatic disease
28
➢Transaminases are elevated
AST, ALT, and GGT
29
elevated AST
1. AST - Aspartate Aminotransferase (SGOT)–a.k.a. Serum Glutamic-Oxaloacetic Transaminase-
–related to glutamic oxalate metabolic pathways
30
elevated ALT
2. ALT - Alanine Aminotransferase (SGPT) –a.k.a. Serum Glutamic-Pyruvic Transaminase-
–part of pyruvate pathway in cell metabolism
31
elevated GGT
3. Gama-Glutamyl Transferase (GGT)- needed for protein synthesis
- useful to detect alcohol-induced liver cell injury and chronic alcoholics
- can detect the slightest degree of cholestasis
- sensitive to biliary obstruction, cholangitis, and cholecystitis
- good marker for pancreatic cancer, prostatic carcinoma, and liver cell
32
high transaminases
| indicates? individually? level? important ratio?
o Indicates damage to hepatocytes from hepatocellular disease
o Not individually proportionally reflective of severity of liver damage
o Up to 300 UI/L --> non-specific
o AST:ALT ratios more informative
- the lower the ratio, the more specific an indicator of hepatic disease
o GGT more indicative of cholestatic disease and alcoholic liver disease
33
albumin levels
synthesized by?
half life?
more indicative of?
specific?
➢ Albumin (low)
oSynthesized “exclusively by hepatocytes”
oHalf-life: 18-20 days
❖More indicative of chronic liver disease
❖Not specific to liver disease:
✓ Malnutrition
✓ Chronic infection
✓ Gut disease
34
PT time
oLiver produces all coagulation factors except?
oPT measures factors:
oVitamin K dependent coagulation factors:
**Prothrombin time (extrinsic and common pathway)**
oLiver produces all coagulation factors except VIII (vascular endothelial cells)
oPT measures factors I, II, V, VII, X
oVitamin K dependent coagulation factors: II, VII, IX, X
oINR is actually PT-INR
35
Viral Hepatitis
➢ All viral hepatitis are RNA virus, except for Hep B (HBV) which is enveloped DNA virus
36
how can Hep damage liver
➢ Hepatocellular damage –> host immune response to viral antigens rather than direct cytopathic effect from virus
oCytotoxic T-cells
oProinflammatory cytokines
oNatural killer cell response
oAntibody-dependent cellular cytotoxicity
37
how can hep infection present?
o Chronic hepatitis can lead to:
➢ Infection may be asymptomatic/symptomatic and acute/chronic
o Patient may clear the virus or virus may become inactive
o Reactivation may occur
o Chronic hepatitis can lead to:
❖ Cirrhosis
❖ Liver failure
❖ Hepatocellular carcinoma.\
❖ Risk factor for immunosuppression
o Chronic hepatitis can lead to:
❖ Carrier state (low levels)
38
Hepatitis B (Hep B; HBV)
| on surfaces? incubation period? chronic in dif demos? vax? reactivation?
➢ Virus can last for up to 7 days on an infected surface
➢ Incubation period: 90 days average
➢ Chronicity:
o90% for infants
o25-50% in children (1-5)
o<5% in adults
➢ Vaccination
o3 doses (initial, 1 month, 6 months)
oSeroconversion necessary
➢ Reactivation
39
hep b tx
➢ Peg- interferon or antivirals such as entecavir and tenofovir
40
acute hep b infection with recovery serology
41
chronic hepb serology
42
serologic test results for vax or 3-6 months following HBIG
HbsAg:-
total anti-HBc:-
IgM anti HBc: -
anti HBs: +
43
serologic results hepb: false positive, resolved infection, low level chronic
HbsAg:-
total anti-HBc: +
IgM anti HBc: -
anti HBs: -
44
serologic test results hepb: chronic infection
HbsAg: +
total anti-HBc: +
IgM anti HBc: -
anti HBs: -
45
serologic results hepb: past infection with recovery and immunity
HbsAg:-
total anti-HBc:+
IgM anti HBc: -
anti HBs: +
46
acute hepb serology
HbsAg:-
total anti-HBc:+
IgM anti HBc: +
anti HBs: -
47
early acute hepb/ vax within recent weeks serology
HbsAg: +
total anti-HBc:-
IgM anti HBc: -
anti HBs: -
48
never infected and susceptable to hepb serology:
HbsAg:-
total anti-HBc:-
IgM anti HBc: -
anti HBs: _
49
Hepatitis C (Hep C; HCV)
| demos? clearence?
➢ Average prevalence in injection drug user = 53%
➢ Baby boomers should be screened, higher risk of having the virus
➢ 15-25% of untreated patients clear the virus
50
HepC chronic?
➢ Has high risk for becoming chronic (75-85%)
o10-20% develop cirrhosis (takes 20-30 years)
oIncreased risk for hepatocellular carcinoma (HCC)
oIncreased risk of death
51
HepC and needle sticks
HCV has higher needlestick transmission rate than HIV
52
hepc vax
none
53
hepC cure/tx?
Cure = undetectable HCV RNA levels after 12 weeks of recommended protease inhibitor therapy
oMavyret (glecaprevir/pibrentasvir)
oEpclusa (sofosbuvir/velpatasvir)
oHarvoni (ledipasvir/sofosbuvir)
54
Hepatitis D (Hep D; HDV)
➢ Usually coinfection with HBV
➢ More severe than HBV alone
➢ Higher risk of fulminant hepatitis
oMassive hepatocellular destruction
55
hep A and E
➢ Infectious hepatitis, fecal-oral transmission
➢ Highly contagious and transmissible
➢ Vaccination available for HAV
56
important hep considerations
* Most carriers aware?
* Hepatitis can be contracted by the dentist?
* liver effects?
* Most carriers of HBV, HCV, HDV are unaware they have hepatitis
* Hepatitis can be contracted by the dentist from an infected patient
* Chronic, active, hepatitis patients may have chronic liver dysfunction:
➢ Increased bleeding
➢ Altered drug metabolism
57
most likely hep to be transmitted to dentist
B followed by C
58
hep A/E risk
little to none in dentistry
59
Viral Hepatitis Considerations
* Reduce oral healthcare worker infection by:
➢ ALL patients considered infectious standard (universal) precautions
➢ HBV vaccination
➢ in the 1990s with public attention to higher population incidences of Hep B, dentists (and other healthcare workers at risk) got the vaccine (3 doses (initial, 1 month, 6 months); then 5 - 10 years later, the HBIg booster was recommended
➢ Most youth get the vaccine today, so there is less public concern;but standard (universal) precautions universal precautions have helped control this risk
60
what to determine with hep pts regarding the dx
➢ Circumstances of infection (age at onset, source of infection)
➢ Status of viral hepatitis
oSerology
oHow/if treated
oViral load
61
screening of high risk pts?
➢ Hep B
➢ Hep C
➢ HIV
➢ Other STDs (HIV, syphilis, gonorrhea, etc.)
62
* Patients with active hepatitis (acute or chronic) dental tx?
➢ Defer all elective dental treatment
➢ If emergency treatment
oConsult physician
oDetermine severity of disease and dental treatment risk
oConsider referral to specialized center
oIsolation may be necessary
63
Patients with history of hepatitis (resolved, chronic inactive) dental tx
➢ Consider risk factors
➢ Consult physician to determine liver status
64
needlestick with hep pt protocol
➢ Consult the physician
➢ Consider hepatitis B immunoglobulin →Why? What kind of immunity? (passive)
65
Viral Hepatitis Oral Manifestations
* Bleeding
* Mucosal jaundice
* Glossitis
* Angular cheilosis
* Extrahepatic immunologic disorders with chronic HCV:
➢ Oral lichen planus
➢ Lymphocytic sialadenitis (Sjögren-like syndrome)
66
AI hep
no virus: autoimmiune dx
67
ages of AI hep
bimodal: adults/kids
kids form more severe
68
tx AI hep
immunosupressants, may require transplant
69
Drug-Induced Liver Disease
* May be a cause as well as consequence of liver disease
* Myriad of drugs may cause liver disease (e.g. APAP, clindamycin, etc.)
70
mechanisms of drug induced liver dx
➢ Direct toxicity to hepatocytes
➢ Production of hepatotoxic metabolites
➢ Accumulation of drug due to altered metabolism
71
nonalcohlic fatty liver dx
still decreased liver function despite no drug or alcoholic cause
72
Alcoholic Liver Disease
* hepatotoxicity?
* Causes?
* Typically takes how long to develop?
* Alcohol as well as its metabolite are hepatotoxic
* Causes inflammation which compounds the liver damage
* Typically takes 10 years of excessive alcohol intake to develop
73
timeline for alcoholic liver dx
➢ Patients first develop fatty liver –reversible
➢ Continual alcohol use and ensuing inflammation can lead to irreversible changes and necrosis
➢ Eventually with continual use, fibrosis and cirrhosis develop –irreversible -leading to hepatic failure
74
complications of alcoholic liver dx
➢ Bleeding tendencies –alcohol can impair platelet function
➢ Unpredictable drug metabolism
➢ Potential impaired immune function
➢ Peripheral neuropathies
➢ Dementia and psychosis
➢ Anorexia
75
alc liver dx chriosis complications
➢ Ascites –hepatorenal syndrome
➢ Esophageal varices –GI bleed
➢ Jaundice
➢ Hepatosplenomegaly
➢ Coagulation disorders
➢ Hypoalbuminemia
➢ Anemia
➢ Neutropenia
➢ Encephalopathy –neurotoxins not removed from liver
76
hepatosplenomegaly of chriosis
oEnlarged spleen due to portal hypertension
oDecreased platelet function
oLeads to thrombocytopenia
77
➢ Coagulation disorders of chriosis
oDecreased synthesis of clotting factors
oImpaired clearance of anticoagulants
oDecreased vitamin K absorption (requires biliary excretion)
78
➢ Anemia of chriosis
oIron deficiency
oMacrocytosis
79
* Identify alcoholic patients via
➢ History
➢ Clinical examination
➢ Detection of odor on breath
➢ Suspicious behavior
➢ Information from family/friend
80
phys consult with alc liver dx
| early/severe dysfunction
* Consult physician to determine the status of liver dysfunction
➢ Early on/mild dysfunction: Liver enzyme induction may increase metabolism of prescribed drugs, limiting their effect
➢ Severe liver dysfunction, drug metabolism may conversely be hindered and drug toxicity is a concern
81
signs of liver failure
82
* Patients with, suspected, active, untreated alcoholic liver disease are not candidates for:
* Patients with, suspected, active, untreated alcoholic liver disease are not
candidates for routine, elective dental treatment
➢ Refer to physician for treatment
83
oral neglect in alcoholics
* Oral neglect is common in those who abuse alcohol
➢ Pts should demonstrate interest and the ability to care for their dentition before
any significant treatment is provided
84
* AST: ALT ratio ≥2 and elevated GGT are suggestive of?
alcoholic liver disease
85
preventing infection in pts with compromised livers?
Maintain good hygiene to avoid spreading of infection given reduced immune capabilities with advanced liver disease whether alcoholic or not
86
hep vs chriosis LFT patterns
87
Alcoholic Liver Disease Oral Manifestations
* Neglect
* Bleeding
* Ecchymoses
* Petechiae
* Glossitis
* Angular cheilosis
* Alcohol odor
* Parotid enlargement
* Xerostomia
88
* A patient with jaundiced mucosal
tissues and breath that is sweet and
musty is associated with:
* A patient with jaundiced mucosal
tissues and breath that is sweet and
musty is associated with liver
failure.
89
General Dental Treatment Considerations in Liver Disease
* Laboratory tests
* Laboratory tests may be needed to evaluate the fitness of the patient for dental treatment(s)
➢ Complete blood count with differential
oPlatelet count is included in a routine CBC
➢ Liver function test which includes:
oAST
oALT
oGGT
oAlbumin
oAlkaline Phosphatase
oBilirubin
➢ Bleeding studies
oPT (PT-INR)
oBleeding time
90
General Dental Treatment Considerations in Liver Disease
* Active liver disease:
➢ Treat patient on emergency basis only
➢ Consult physician to determine status
➢ If severe liver disease and requires emergency treatment
oConsider referral to specialized center
91
General Dental Treatment Considerations in Liver Disease
* History of liver disease
➢ Age at onset
➢ Consult physician to determine status and medication usage
➢ Compensated disease or decompensated disease
➢ Assess other end-organ damage
oGall bladder
oRenal
oCardiovascular
oHematologic disease (anemia, bleeding and prothrombotic states –failure to clear coagulation factors –risk for Disseminated Intravascular Coagulation (DIC)
92
preop considerations to deal with bleeding complications in a
patient with significant liver disease.
oConsult with physician concerning liver disease status
❖ Defer if decompensated
oReview medications to assess other possible medication-related bleeding risk
❖Example: anticoagulants
o Request relevant labs and check results to confirm if safe to proceed
o If urgent and dental treatment is necessary and cannot be deferred, refer to specialized care where other agents available to deal with a serious bleed
❖ Vitamin K
❖ Fresh frozen plasma (contains all coagulation factors)
❖ Platelet transfusion
93
peri/intraop strategies to deal with bleeding complications in a
patient with significant liver disease.
oPerform extractions as atraumatically as possible
oIf performing a scaling and root planing, do one tooth at a time rather than an entire quadrant at a time
oHave local hemostatic agents available
❖ Surgicel, Gelfoam
❖ Topical thrombin
❖ Tranexamic acid
❖ Bone wax,
❖ Electrocautery
❖ Silver nitrate sticks
❖ Aminocaproic acid (Amicar) rinse
oPlace sutures in all extraction sites
94
postop strategies to deal with bleeding complications in a
patient with significant liver disease.
➢ Have patient sit in dental chair for 20 minutes after procedure and assess that local hemostasis is adequate before sending patient home
➢ Explain verbally and have written post-op instructions available for the patient
➢ Do not prescribe NSAIDs for pain management
➢ Can give acetaminophen up to 2g daily in most cases for pain management
➢ Supply patient with gauze to take home
➢ Reinforce the need to maintain clot in place (no straws, no spitting, avoid talking and maintain soft diet for 2-3 days)
➢ Inform patient to call should bleeding persist; may need to go hospital
95
General Dental Treatment Considerations in Liver Disease
* Antibiotic prophylaxis
* Antibiotic prophylaxis prior to procedures is not required if no oral infection is present
* Patients with SEVERE LIVER DISEASE may need antibiotic prophylaxis (coverage) for invasive/surgical procedures due to decreased immune function
➢ Weight risk/benefit ratio
Impairment of drug metabolism vs immune impairment
96
General Dental Treatment Considerations in
Liver Disease: DRUGS
Minimize use of drugs metabolized by liver
➢Local Anesthetic
➢Analgesics
➢Sedatives
➢Antimicrobials
97
➢Local Anesthetic with liver dx
o metab in liver
o increased duration and half life
o esters not as effective but also no liver metabolism
98
➢Analgesics and liver dx
oLimit acetominphen (APAP). recommended maximum daily dose for an adult is three to four grams
oHigher doses may lead to toxicity, including liver failure
oNSAIDs should be avoided.
oIf opioids are necessary, hydromorphone is preferred choice- glucuronidation
oAvoid hydrocodone, oxycodone-unpredictable metabolism
99
➢Sedatives with liver dx
oAvoid benzodiazepines
oLorazepam –potentially used due to lower half life
oN2O safer, if possible
100
➢Antimicrobials with liver dx
oAvoid metronidazole, tetracycline, doxycycline- porr metabolism
oAvoid azole antifungals (fluconazole)
oPossible issue with clindamycin.
oDo not drink alcohol with antibiotics
–metronidazole and 2nd and 3rd generation cephalosporins -
Disulfiram effect
101
Cautionary Dental Treatment Considerations in Liver Disease
* Caution with hypertension
➢ Portal hypertension is a complication of cirrhosis
o BP can be significantly elevated with portal hypertension
o Limit epinephrine (epi)
o Do not use retraction cord with epinephrine
o thrombocytopenia (from platelet sequestration in the spleen)
102
Cautionary Dental Treatment Considerations in Liver Disease
* Caution with immunosuppression
Patients with SEVERE LIVER DISEASE may need antibiotic prophylaxis (coverage) for invasive/surgical procedures due to decreased immune function
➢ Weight risk : benefit ratio
i.e., Impairment of drug metabolism : immune impairment
MED COMP PTS
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