Hepatic Disease Flashcards
(92 cards)
1
Q
Where is the liver?
A
located in the R upper quadrant
2
Q
What is the largest internal organ?
A
liver
3
Q
Where does the liver get the dual blood supply from?
A
➢ ~ 20 % Hepatic artery - oxygenated blood
➢ 80% Portal vein – nutrients
4
Q
What is the common hepatic duct?
A
- 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
5
Q
What is the common bile duct?
A
- 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
6
Q
What are the roles of the hepatic veins?
A
drain venous blood from liver to inferior vena cava and on to the right
7
Q
What is the role of the hepatic artery?
A
provides oxygen and nutrition to liver tissues
8
Q
What is the role of the 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
9
Q
What is the function of the hepatocytes?
A
➢ Synthesizes proteins
- Immunoglobulins
- Albumin
- coagulation factors (most come from the liver)
- carrier proteins
- growth factors
- hormones
➢ Produces bile for digestion (via bilirubin)
➢ Produces cholesterol for fat storage
➢ Regulates nutrients
➢ Prepares drugs for excretion
➢ Responsible for drug conjugation and metabolism
10
Q
bilirubin transported to liver by being bound to ___________
A
albumin
(unconjugated form)
11
Q
bilirubin is from breakdown of…
A
RBCs
12
Q
Liver conjugates bilirubin by unbinding the protein binding it to glucose; this conjugated form is in _________
A
bile
13
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.
14
Q
What does increased bilirubin cause/what are the signs of bilirubin increase?
A
jaundice, fatigue, cutaneous itch, discolored urine, discolored feces
15
Q
What type of metabolism is done in the liver?
A
- Bilirubin conjugation
- Phase I – cytochrome P450; can produce toxic metabolites
- Phase II – conjugation (glucuronidation, sulfation, inactivation by glutathione, etc.)
16
Q
What are the types of damage the liver can have?
A
➢ Hepatocellular (inflammation and injury)
➢ Cholestatic (obstructive)
➢ Mixed
➢ Cirrhosis (fibrotic, end-stage); acute or chronic
➢ Neoplastic
17
Q
What are the types of liver disease?
A
➢ Viral hepatitis (A, B, C, D, E, non- A-E)
➢ Immune and Autoimmune (primary biliary cholangitis, autoimmune hepatitis, GVHD)
➢ Genetic (α1-trypsin deficiency, Wilson disease)
➢ Non-alcoholic fatty liver (obesity, insulin resistance, lipodystrophy)
➢ Cholestatic syndromes
➢ Systemic disease with liver involvement (sarcoidosis, amyloidosis, TB, glycogen storage disease)
➢ Drug-induced liver disease
➢ Hepatocellular carcinoma
➢ Masses, cysts, abscess
18
Q
What are the signs of liver damage?
A
➢ Jaundice
➢ Ascites
➢ Edema
➢ GI bleed
➢ Dark urine
➢ Light stool
➢ Mental confusion
➢ Xanthelasma
➢ Spider angiomas
➢ Palmar erythema
➢ Asterixis
➢ Hyperpigmentation
19
Q
What are the symptoms of liver damage?
A
➢ Appetite loss
➢ Bloating
➢ Nausea
➢ RUQ pain
➢ Fatigue
➢ Mental confusion
20
Q
What is xanthelasma?
A
fatty deposits on the skin (eyes)
21
Q
What are unique findings associated with liver disease?
A
- Xanthelasma
- Spider angiomas
- Asterixis
22
Q
What is asterixis?
A
- a.k.a. flapping tremor
- classic sign in hepatic encephalopathy (HE)
- jerky movements when hands are extended at wrists
23
Q
What is hepatic encephalopathy (HE)?
A
- a syndrome of altered neurologic function related to dysregulation of metabolism seen almost exclusively in patients with severe liver disease
- can be a chronic problem in patients with cirrhosis
- acute exacerbations are rarely fatel
24
Q
What kind of blood tests might a patient be referring to when they say they had a “blood test”?
A
- Complete Blood Count (CBC)
- Comprehensive Metabolic Panel (CMP)
- Multiple others available for specific patient evaluations
— lipid panel
— VDRL
— PSA (prostate specific antigen)
— SARS Ag, SARS Ab, HIV, Hep B, etc.
— bleeding times
— et cetera
25
What is a complete blood count?
* 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
--- infection
--- anemia
--- leukemia
--- lymphoma
--- neutropenia
--- etc.
26
What is a comprehensive metabolic panel (CMP)?
* 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
27
What types of tests are available for liver function?
* Bilirubin
* Alkaline phosphatase (ALP)
* Transaminases
--- Aspartate amino transferase (AST or SGOT)
--- Alanine amino transferase (ALT or SGPT)
--- Gama-Glutamyl Transferase (GGT)
* Albumin
* Globulin
28
If the bilirubin level are high unconjugated (indirect), what does that mean?
| he didn't talk much about this
❖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)
29
If the bilirubin level are high conjugated (direct), what does that mean?
| he didn't talk much about this
❖Increased SERUM indicative of liver disease
❖Water-soluble, excreted by kidney
❖All URINE bilirubin is conjugated
30
What does a high alkaline phosphatase tell us?
o altered in myriad of diseases especially bone neoplasms
o not specific to liver disease,
o may indicate cholestatic disease
| alkaline phosphatase involved in bone metabolism
31
What does a high bilirubin test tell us?
o Product of heme breakdown
o Increased total bilirubin, increased severity of liver injury
32
What does the AST - Aspartate Aminotransferase (SGOT) tell us?
–a.k.a. Serum Glutamic-Oxaloacetic Transaminase
- related to glutamic oxalate metabolic pathways
33
What does the ALT - Alanine Aminotransferase (SGPT) tell us?
–a.k.a. Serum Glutamic-Pyruvic Transaminase
– part of pyruvate pathway in cell metabolism
34
What does the Gama Glutamyl transferase (GGT) tell us?
- 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 ce
35
What does a high transaminase mean?
| AST (SGOT), ALT (SGPT), GGT
- Indicates damage to hepatocytes from hepatocellular disease
- Not individually proportionally reflective of severity of liver damage
- Up to 300 UI/L --> non-specific
36
AST:ALT ratios more informative: the _______ the ratio, the more specific an indicator of hepatic disease
lower
37
GGT more indicative of ___________ disease and __________ disease
cholestatic
alcoholic liver
38
What does a low albumin test tell us?
❖More indicative of chronic liver disease
❖Not specific to liver disease
✓ Malnutrition
✓ Chronic infection
✓ Gut disease
39
Where is albumin synthesized?
exclusively by hepatocytes
o Half-life: 18-20 days
40
Liver produces all coagulation factors except...
VIII (vascular endothelial cells)
41
PT measures which factors?
I, II, V, VII, X
42
Vitamin K dependent coagulation factors:
II, VII, IX, X
43
All viral hepatitis are RNA virus except....
HepB which is DNA
44
What is hepatocellular damage?
host immune response to viral antigens rather
than direct cytopathic effect from virus
o Cytotoxic T-cells
o Proinflammatory cytokines
o Natural killer cell response
o Antibody-dependent cellular cytotoxicity
| Caused by viral hepatitis
45
What is viral hepatitis?
➢ Infection may be asymptomatic/symptomatic and acute/chronic
o Patient may clear the virus or virus may become inactive
o Reactivation may occur
o When chronic infection but asymptomatic
❖ Carrier state (low levels)
46
What can chronic hepatitis lead to?
o Chronic hepatitis can lead to
❖ Cirrhosis
❖ Liver failure
❖ Hepatocellular carcinoma.\
❖ Risk factor for immunosuppression
47
How long can HepB last on an infected surface?
up to 7 days
48
Incubation period of HepB
90 days average
49
Chronicity of HepB:
o 90% for infants
o 25-50% in children (1-5)
o <5% in adults
50
Vaccination for HepB:
o 3 doses (initial, 1 month, 6 months)
o Seroconversion necessary - What does this mean?
51
Prevalence of HepC in injection drug users:
35%
52
Who should be screened bc of higher risk of HepC?
baby boomers
53
What are characteristics of HepC?
➢ Has high risk for becoming chronic (75-85%)
o 10-20% develop cirrhosis (takes 20-30 years)
o Increased risk for hepatocellular carcinoma (HCC)
o Increased risk of death
➢ HCV has higher needlestick transmission rate than HIV
➢ No vaccine
➢ Cure = undetectable HCV RNA levels after 12 weeks of recommended protease
inhibitor therapy
o Mavyret (glecaprevir/pibrentasvir)
o Epclusa (sofosbuvir/velpatasvir)
o Harvoni (ledipasvir/sofosbuvir)
54
People can be _____ carriers of HepC
chronic
55
What are characteristics of HepD?
➢ Usually coinfection with HBV
➢ More severe than HBV alone
➢ Higher risk of fulminant hepatitis
o Massive hepatocellular destruction
56
What are characteristics of HepA and HepE?
➢ Infectious hepatitis, fecal-oral transmission
➢ Highly contagious and transmissible
➢ Vaccination available for HAV
57
What are viral hepatitis considerations?
* 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
* Little to no risk exists for transmission of HAV, HEV, and non-A-E hepatitis viruses
58
Hep __ is most likely viral hepatitis to be transmitted occupationally to a dental
health care worker, followed by Hep __
1: HepB
2: HepC
59
How to reduce oral healthcare worker infection of viral hepatitis:
➢ 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 do you need to determine of viral hepatitis?
➢ Circumstances of infection (age at onset, source of infection)
➢ Status of viral hepatitis
o Serology
o How/if treated
o Viral load
61
What to do with patients with active hepatitis (acute or chronic):
➢ Defer all elective dental treatment
➢ If emergency treatment
o Consult physician
o Determine severity of disease and dental treatment risk
o Consider referral to specialized center
o Isolation may be necessary
62
What to do with patients with history of hepatitis (resolved, chronic inactive)
➢ Consider risk factors
➢ Consult physician to determine liver status
63
What to do if needlestick?
➢ Consult the physician
➢ Consider hepatitis B immunoglobulin → Why? What kind of immunity?
64
What are oral manifestations of viral hepatitis?
* Bleeding
* Mucosal jaundice
* Glossitis
* Angular cheilosis
* Extrahepatic immunologic disorders with chronic HCV
➢ Oral lichen planus
➢ Lymphocytic sialadenitis (Sjögren-like syndrome)
65
Types of autoimmune hepatitis:
AIH-1: adult predominant
AIH-2: pediatric predominant (more severe)
66
probably need to know this?
67
What is 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.)
68
What are the mechanisms of drug-induced liver disease?
* Mechanisms
➢ Direct toxicity to hepatocytes
➢ Production of hepatotoxic metabolites
➢ Accumulation of drug due to altered metabolism
69
What is nonalcoholic fatty liver disease?
- not related to alcohol
- decreased hepatic function
70
What is alcoholic liver disease?
* 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
➢ 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
71
What are complications of alcoholic liver disease?
➢ Bleeding tendencies – alcohol can impair platelet function
➢ Unpredictable drug metabolism
➢ Potential impaired immune function
➢ Peripheral neuropathies
➢ Dementia and psychosis
➢ Anorexia
72
What are complications of cirrhosis?
➢ Ascites – hepatorenal syndrome
➢ Esophageal varices – GI bleed
➢ Jaundice
➢ Hepatosplenomegaly
o Enlarged spleen due to portal hypertension
o Decreased platelet function
o Leads to thrombocytopenia
➢ Coagulation disorders
o Decreased synthesis of clotting factors
o Impaired clearance of anticoagulants
o Decreased vitamin K absorption (requires biliary excretion)
➢ Hypoalbuminemia
➢ Anemia
o Iron deficiency
o Macrocytosis
➢ Neutropenia
➢ Encephalopathy – neurotoxins not removed from liver
73
How to ID alcoholic patients:
➢ History
➢ Clinical examination
➢ Detection of odor on breath
➢ Suspicious behavior
➢ Information from family/friend
74
What are the effects of early on/mild liver dysfunction?
Liver enzyme induction may increase metabolism of prescribed drugs, limiting their effect
75
What are the effects of sever liver dysfunction?
drug metabolism may conversely be hindered and drug toxicity is a concern
76
AST:ALT ratio greater than 2 and elevated GGT suggestive of what?
alcoholic liver disease
77
What are alcoholic liver disease considerations?
* Patients with, suspected, active, untreated alcoholic liver disease are not
candidates for routine, elective dental treatment
➢ Refer to physician for treatment
* 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
* Maintain good hygiene to avoid spreading of infection given reduced immune
capabilities with advanced liver disease whether alcoholic or not.
78
idk if we need to know this?
79
Oral manifestations of alcoholic liver disease:
* Neglect
* Bleeding
* Ecchymoses
* Petechiae
* Glossitis
* Angular cheilosis
* Alcohol odor
* Parotid enlargement
* Xerostomia
* A patient with jaundiced mucosal
tissues and breath that is sweet and
musty is associated with liver
failure.
* Alcohol abuse is a strong risk factor
for oral squamous cell carcinoma
80
What is the number one abused drug in terms of emergency room visits, hospital
admission, family violence, and other social problems?
alcohol
81
What are general dental treatment considerations in liver disease?
* Laboratory tests may be needed to evaluate the fitness of the patient for dental
treatment(s)
➢ Complete blood count with differential
o Platelet count is included in a routine CBC
➢ Liver function test which includes:
o AST
o ALT
o GGT
o Albumin
o Alkaline Phosphatase
o Bilirubin
➢ Bleeding studies
o PT (PT-INR)
o Bleeding time
82
What to do if patient has active liver disease?
➢ Treat patient on emergency basis only
➢ Consult physician to determine status
➢ If severe liver disease and requires emergency treatment
o Consider referral to specialized center
83
What to do if patient has 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
o Gall bladder
o Renal
o Cardiovascular
o Hematologic disease (anemia, bleeding and prothrombotic states – failure to clear
coagulation factors –risk for Disseminated Intravascular Coagulation (DIC)
84
What are PRE- operative strategies to deal with bleeding complications in a patient with significant liver disease?
o Consult with physician concerning liver disease status
❖ Defer if decompensated
o Review 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
85
What are PERI/INTRA- operative strategies to deal with bleeding complications in a patient with significant liver disease?
o Perform extractions as atraumatically as possible
o If performing a scaling and root planing, do one tooth at a time rather than
an entire quadrant at a time
o Have local hemostatic agents available
❖ Surgicel, Gelfoam
❖ Topical thrombin
❖ Tranexamic acid
❖ Bone wax,
❖ Electrocautery
❖ Silver nitrate sticks
❖ Aminocaproic acid (Amicar) rinse
o Place sutures in all extraction sites
86
What are POST- operative 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
87
Is antibiotic prophylaxis needed for patients with liver disease?
* 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
88
Minimize or maximize use of drugs metabolized by liver?
MINIMIZE
➢Local Anesthetic
➢Analgesics
➢Sedatives
➢Antimicrobials
89
Why minimize analgesics in patients with liver disease?
o Limit acetominphen (APAP). recommended
maximum daily dose for an adult is three to
four grams
o Higher doses may lead to toxicity,
including liver failure
o NSAIDs should be avoided. Why?
o If opioids are necessary, hydromorphone is
preferred choice- glucuronidation
o Avoid hydrocodone, oxycodone-
unpredictable metabolism
90
What sedatives should be avoided in patients with liver disease?
o Avoid benzodiazepines
o Lorazepam – potentially used. Why? --> smaller 1/2 life
o N2O safer, if possible
91
Why should you avoid metronidazole in patients with liver disease?
Do not drink alcohol with antibiotics
– metronidazole and 2nd and 3rd
generation cephalosporins -
Disulfiram effect
92
Why should you be cautious with hypertension in patients with liver disease?
➢ 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)
