Gastrointestinal and Hepatic Disease Part 1 Flashcards
1
Q
Liver
A
- Largest internal organ; located in the R upper quadrant
2
Q
Liver
* Largest internal organ; located in the R upper quadrant
* Dual blood supply
(2)
A
➢ ~ 20 % Hepatic artery - oxygenated blood
➢ 80% Portal vein –nutrients
3
Q
Common Hepatic Duct
- — forms the common hepatic duct
- drains — from the liver
- fxn (2)
A
left and right hepatic ducts
bile
transports waste from the liver and aids in digestion by releasing bile
4
Q
Common Bile Duct
- carries bile from
- part of the biliary duct system; formed where the
A
the liver and the gallbladder through the pancreas and into the
duodenum
ducts from the liver and gallbladder are
joined
5
Q
Hepatic Veins –
A
drain venous blood from liver to inferior vena cava and on to the right
6
Q
Hepatic Artery –
A
provides oxygen and nutrition to liver tissues
7
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
8
Q
Function of hepatocytes
➢ Synthesizes proteins
(6)
A
- Immunoglobulins
- Albumin
- coagulation factors
- carrier proteins
- growth factors
- hormones
9
Q
Function of hepatocytes
(4)
A
➢ 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
10
Q
Bilirubin levels escalate from:
(3)
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.
11
Q
➢ Increased bilirubin – (5)
A
jaundice,
fatigue,
cutaneous itch,
discolored urine,
discolored feces (?)
12
Q
Function of hepatocytes
➢ Regulates nutrients
(4)
A
- glucose
- glycogen
- lipids
- amino acids
13
Q
Function of hepatocytes
➢ Regulates –
➢ Prepares drugs for –
➢ Responsible for (2)
A
nutrients
excretion
drug conjugation and metabolism
14
Q
➢ Responsible for drug conjugation and metabolism
oBilirubin conjugation
oPhase I –
oPhase II –
A
cytochrome P450; can produce toxic metabolites
conjugation (glucuronidation, sulfation, inactivation by
glutathione, etc.)
15
Q
Types of damage
(5)
A
➢ Hepatocellular (inflammation and injury)
➢ Cholestatic (obstructive)
➢ Mixed
➢ Cirrhosis (fibrotic, end-stage); acute or chronic
➢ Neoplastic
16
Q
Types of liver disease
(9)
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
17
Q
Signs
A
➢ Jaundice
➢ Ascites
➢ Edema
➢ GI bleed
➢ Dark urine
➢ Light stool
➢ Mental confusion
➢ Xanthelasma
➢ Spider angiomas
➢ Palmar erythema
➢ Asterixis
➢ Hyperpigmentation
18
Q
Symptoms
A
➢ Appetite loss ֎
➢ Bloating
➢ Nausea
➢ RUQ pain
➢ Fatigue
➢ Mental confusion
19
Q
Asterixis
(3)
A
- a.k.a. flapping tremor
- classic sign in hepatic encephalopathy (HE)
- jerky movements when hands are extended at wrists.
20
Q
hepatic encephalopathy (HE)
A
a syndrome of altered neurologic function related to dysregulation of metabolism seen almost exclusively in patients with severe liver disease
21
Q
HE can be a chronic problem in patients with
A
cirrhosis, managed medically to varying degrees of success, punctuated with occasional exacerbations
22
Q
although these acute exacerbations of HE are rarely fatal, they are a frequent cause of
A
hospitalizations among patients with cirrhosis
23
Q
Blood Tests
(2)
A
*Complete Blood Count (CBC)
*Comprehensive Metabolic Panel (CMP)
Multiple others available for specific patient evaluations
24
Q
Complete Blood Count (CBC)
(3)
A
- evaluate the cells that circulate in blood
- indicator of overall health
- may detect a variety of diseases and conditions
25
Multiple others available for specific patient evaluations
(6)
* - lipid panel
* - VDRL
* - PSA (prostate specific antigen)
* - SARS Ag, SARS Ab, HIV, Hep B, etc.
* - bleeding times
* - et cetera
26
evaluate the cells that circulate in blood
(3)
red blood cells (RBCs)
white blood cells (WBCs)
platelets (PLTs)
27
may detect a variety of diseases and conditions
(5)
- infection
- anemia
- leukemia
- lymphoma
- neutropenia
- etc.
28
Comprehensive Metabolic Panel (CMP)
(3)
* aka chemical screen or,
SMAC 14 (Sequential Multiple Analysis –Computer)
* consists of 14 blood tests which serves as an initial broad medical screening tool
* there are also SMAC 8, 12, 16 and 20 variants
29
Comprehensive Metabolic Panel (CMP)
Includes
(5)
- General tests
- Kidney function assessment
- Electrolytes
- Protein tests
- Liver function assessment
30
Liver Function Tests
(5)
*Bilirubin
*Alkaline phosphatase (ALP)
*Transaminases
*Albumin
*Globulin
31
Transaminases
(3)
- Aspartate amino transferase (AST or SGOT)
- Alanine amino transferase (ALT or SGPT)
- Gama-Glutamyl Transferase (GGT)
32
Liver Function Test
➢ Bilirubin (high)
(2)
oProduct of heme breakdown
oIncreased total bilirubin, increased severity of liver injury
33
Unconjugated (indirect)
(3)
❖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)
34
Conjugated bilirubin (direct)
(3)
❖Increased SERUM indicative of liver disease
❖Water-soluble, excreted by kidney
❖All URINE bilirubin is conjugated
35
Alkaline phosphatase (high)
(3)
oaltered in myriad of diseases especially bone neoplasms
onot specific to liver disease,
omay indicate cholestatic disease
36
1. AST - Aspartate Aminotransferase (SGOT)
–a.k.a. Serum Glutamic-Oxaloacetic Transaminase-
–related to glutamic oxalate metabolic pathways
37
2. ALT - Alanine Aminotransferase (SGPT)
–a.k.a. Serum Glutamic-Pyruvic Transaminase-
–part of pyruvate pathway in cell metabolism
38
3. Gama-Glutamyl Transferase (GGT)
- needed for --- synthesis
- useful to detect ---
- can detect the slightest degree of ---
- sensitive to (3)
- good marker for(3)
protein
alcohol-induced liver cell injury and chronic alcoholics
cholestasis
biliary obstruction, cholangitis, and cholecystitis
pancreatic cancer, prostatic carcinoma, and liver cell carcinoma
39
Transaminases (high)
oTypes (3)
oIndicates --
oNot individually proportionally reflective of --
oUp to 300 UI/L -->
oAST:ALT ratios more informative
- the lower the ratio, the more --
oGGT more indicative of (2)
AST (SGOT), ALT (SGPT), GGT
damage to hepatocytes from hepatocellular disease
severity of liver damage
non-specific
specific an indicator of hepatic disease
cholestatic disease and alcoholic liver disease
40
Liver Function Test
➢ Albumin (low)
(3)
oSynthesized “exclusively by hepatocytes”
oHalf-life: 18-20 days
oHypoalbuminemia
41
oHypoalbuminemia
(2)
❖More indicative of chronic liver disease
❖Not specific to liver disease
✓ Malnutrition
✓ Chronic infection
✓ Gut disease
42
Prothrombin time (extrinsic and common pathway)
oLiver produces all coagulation factors except --
oPT measures factors (5)
oVitamin K dependent coagulation factors: (4)
oINR is actually ---
VIII (vascular endothelial cells)
I, II, V, VII, X
II, VII, IX, X
PT-INR
43
All viral hepatitis are RNA virus, except for
Hep B (HBV) which is
enveloped DNA virus
44
Hepatocellular damage –> host immune response to viral antigens rather
than direct cytopathic effect from virus
(4)
oCytotoxic T-cells
oProinflammatory cytokines
oNatural killer cell response
oAntibody-dependent cellular cytotoxicity
45
Infection may be asymptomatic/symptomatic and acute/chronic
(4)
oPatient may clear the virus or virus may become inactive
oReactivation may occur
oChronic hepatitis can lead to
oWhen chronic infection but asymptomatic
46
Chronic hepatitis can lead to
(4)
❖ Cirrhosis
❖ Liver failure
❖ Hepatocellular carcinoma.\
❖ Risk factor for immunosuppression
47
When chronic infection but asymptomatic
(1)
❖ Carrier state (low levels)
48
Viral Hepatitis
(4)
* Serum hepatitis, blood-borne
* Parenteral, intimate and sexual exposure
* Populations at risk?
* Coinfection?
49
Hepatitis B (Hep B; HBV)
➢ Virus can last for up to -- days on an infected surface
➢ Incubation period: -- days average
➢ Reactivation
➢ Peg-
7
90
interferon or antivirals such as entecavir and tenofovir
50
HBV
➢ Chronicity:
--% for infants
--% in children (1-5)
--% in adults
o90
o25-50
o<5
51
Vaccination
(2)
o3 doses (initial, 1 month, 6 months)
oSeroconversion necessary - What does this mean?
52
Hepatitis C (Hep C; HCV)
➢ Average prevalence in injection drug user = --
➢ --- should be screened, higher risk of having the virus
➢ --% of untreated patients clear the virus
➢ Has high risk for becoming ---
➢ HCV has higher --- transmission rate than HIV
➢ No ---
➢ Cure =
53%
Baby boomers
15-25
chronic (75-85%)
needlestick
vaccine
undetectable HCV RNA levels after 12 weeks of recommended protease
inhibitor therapy
53
➢ Has high risk for becoming chronic (75-85%)
(3)
o10-20% develop cirrhosis (takes 20-30 years)
oIncreased risk for hepatocellular carcinoma (HCC)
oIncreased risk of death
54
➢ Cure = undetectable HCV RNA levels after 12 weeks of recommended protease
inhibitor therapy
(3)
oMavyret (glecaprevir/pibrentasvir)
oEpclusa (sofosbuvir/velpatasvir)
oHarvoni (ledipasvir/sofosbuvir)
55
Hepatitis D (Hep D; HDV)
(3)
➢ Usually coinfection with HBV
➢ More severe than HBV alone
➢ Higher risk of fulminant hepatitis
oMassive hepatocellular destruction
56
Hepatitis A and E
(3)
➢ Infectious hepatitis, fecal-oral transmission
➢ Highly contagious and transmissible
➢ Vaccination available for HAV
57
Viral Hepatitis Considerations
* Most carriers of (3) are unaware they have hepatitis
* Hepatitis can be contracted by
* Chronic, active, hepatitis patients may have
HBV, HCV, HDV
the dentist from an infected patient
chronic liver dysfunction
58
Chronic, active, hepatitis patients may have chronic liver dysfunction
(2)
➢ Increased bleeding
➢ Altered drug metabolism
59
Hep --- is most likely viral hepatitis to be transmitted occupationally to a dental
health care worker, followed by Hep
B
C
60
Little to no risk exists for transmission of
HAV, HEV, and non-A-E hepatitis viruses
61
Reduce oral healthcare worker infection by:
(2)
➢ ALL patients considered infectious standard (universal) precautions
➢ HBV vaccination
62
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
63
Most youth get the vaccine today, so there is less public concern;
but
standard (universal) precautions universal precautions have helped control this
risk
64
Viral Hepatitis Considerations
* Determine
(2)
➢ Circumstances of infection (age at onset, source of infection)
➢ Status of viral hepatitis
oSerology
oHow/if treated
oViral load
65
Consider screening for patients in high-risk categories
(4)
➢ Hep B
➢ Hep C
➢ HIV
➢ Other STDs (HIV, syphilis, gonorrhea, etc.)
66
Patients with active hepatitis (acute or chronic)
(2)
➢ 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
67
Patients with history of hepatitis (resolved, chronic inactive)
(2)
➢ Consider risk factors
➢ Consult physician to determine liver status
68
Needlestick
(2)
➢ Consult the physician
➢ Consider hepatitis B immunoglobulin →Why? What kind of immunity?
69
Viral Hepatitis Oral Manifestations
(5)
* Bleeding
* Mucosal jaundice
* Glossitis
* Angular cheilosis
* Extrahepatic immunologic disorders with chronic HCV
➢ Oral lichen planus
➢ Lymphocytic sialadenitis (Sjögren-like syndrome)
70
Drug-Induced Liver Disease
* May be a cause as well as consequence of
* Myriad of drugs may cause
liver disease
liver disease (e.g. APAP, clindamycin, etc.)
71
Drug-Induced Liver Disease
Mechanisms
(3)
➢ Direct toxicity to hepatocytes
➢ Production of hepatotoxic metabolites
➢ Accumulation of drug due to altered metabolism
72
Alcoholic Liver Disease
* Alcohol as well as its metabolite are
* Causes --- which compounds the liver damage
* Typically takes --- years of excessive alcohol intake to develop
hepatotoxic
inflammation
10
73
Typically takes 10 years of excessive alcohol intake to develop
➢ Patients first develop
➢ Continual alcohol use and ensuing inflammation can lead to
➢ Eventually with continual use,
fatty liver –reversible
irreversible changes
and necrosis
fibrosis and cirrhosis develop –irreversible -
leading to hepatic failure
74
Alcoholic Liver Disease
Complications
(6)
➢ Bleeding tendencies –alcohol can impair platelet function
➢ Unpredictable drug metabolism
➢ Potential impaired immune function
➢ Peripheral neuropathies
➢ Dementia and psychosis
➢ Anorexia
75
Alcoholic Liver Disease
* Complications of cirrhosis
(5)
➢ Ascites –hepatorenal syndrome
➢ Esophageal varices –GI bleed
➢ Jaundice
➢ Hepatosplenomegaly
➢ Coagulation disorders
76
Hepatosplenomegaly
(3)
oEnlarged spleen due to portal hypertension
oDecreased platelet function
oLeads to thrombocytopenia
77
Coagulation disorders
(3)
oDecreased synthesis of clotting factors
oImpaired clearance of anticoagulants
oDecreased vitamin K absorption (requires biliary excretion)
78
Complications of cirrhosis
(4)
➢ Hypoalbuminemia
➢ Anemia
➢ Neutropenia
➢ Encephalopathy –neurotoxins not removed from liver
79
➢ Anemia
(2)
oIron deficiency
oMacrocytosis
80
Alcoholic Liver Disease
* Identify alcoholic patients via
(5)
➢ History
➢ Clinical examination
➢ Detection of odor on breath
➢ Suspicious behavior
➢ Information from family/friend
81
Consult physician to determine the status of liver dysfunction
➢ Early on/mild dysfunction:
➢ Severe liver dysfunction,
Liver enzyme induction may increase metabolism of
prescribed drugs, limiting their effect
drug metabolism may conversely be hindered and drug
toxicity is a concern
82
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
83
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 ≥--- and elevated GGT are suggestive of alcoholic liver disease
2
85
* Maintain good hygiene to avoid
spreading of infection given reduced immune
capabilities with advanced liver disease whether alcoholic or not.
86
Alcoholic Liver Disease Oral Manifestations
* Neglect
* Bleeding
* Ecchymoses
* Petechiae
* Glossitis
* Angular cheilosis
* Alcohol odor
* Parotid enlargement
* Xerostomia
87
* A patient with jaundiced mucosal
tissues and breath that is
sweet and
musty is associated with liver
failure.
88
* Alcohol abuse is a strong risk factor
for
oral squamous cell carcinoma
89
*--- is the number one abused drug in terms of emergency room visits, hospital
admission, family violence, and other social problems
Alcohol Abuse
90
General Dental Treatment Considerations in Liver Disease
* Laboratory tests may be needed to evaluate the fitness of the patient for dental
treatment(s)
(2)
➢ Complete blood count with differential
➢ Liver function test which includes:
91
➢ Complete blood count with differential
oPlatelet count is included in a routine CBC
92
Liver function test which includes:
(6)
oAST
oALT
oGGT
oAlbumin
oAlkaline Phosphatase
oBilirubin
93
Laboratory tests may be needed to evaluate the fitness of the patient for dental
treatment(s)
➢ Bleeding studies
(2)
oPT (PT-INR)
oBleeding time
94
Active liver disease:
(3)
➢ Treat patient on emergency basis only
➢ Consult physician to determine status
➢ If severe liver disease and requires emergency treatment
oConsider referral to specialized center
95
History of liver disease
(4)
➢ Age at onset
➢ Consult physician to determine status and medication usage
➢ Compensated disease or decompensated disease
➢ Assess other end-organ damage
96
Assess other end-organ damage
(4)
oGall bladder
oRenal
oCardiovascular
oHematologic disease (anemia, bleeding and prothrombotic states –failure to clear
coagulation factors –risk for Disseminated Intravascular Coagulation (DIC)
97
PRE
oConsult with --- concerning liver disease status
❖ Defer if ---
oReview --- to assess other possible medication-related bleeding
risk
❖Example: ---
oRequest relevant --- and check results to confirm if safe to proceed
oIf urgent and dental treatment is necessary and cannot be deferred, refer to
specialized care where other agents available to deal with a serious bleed
(3)
physician
decompensated
medications
anticoagulants
labs
❖ Vitamin K
❖ Fresh frozen plasma (contains all coagulation factors)
❖ Platelet transfusion
98
➢ PERI/INTRA
oPerform --- as atraumatically as possible
oIf performing a scaling and root planing, do ---
oHave --- available
extractions
one tooth at a time rather than
an entire quadrant at a time
local hemostatic agents
❖ Surgicel, Gelfoam
❖ Topical thrombin
❖ Tranexamic acid
❖ Bone wax,
❖ Electrocautery
❖ Silver nitrate sticks
❖ Aminocaproic acid (Amicar) rinse
oPlace sutures in all extraction sites
99
➢ POST
➢ Have patient sit in dental chair for --- 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 --- for pain management
➢ Can give --- up to 2g daily in most cases for pain management
➢ Supply patient with --- to take home
➢ Reinforce the need to maintain ---
➢ Inform patient to call should --- persist; may need to go hospital
20
NSAIDs
acetaminophen
gauze
clot in place (no straws, no spitting, avoid
talking and maintain soft diet for 2-3 days)
bleeding
100
General Dental Treatment Considerations in Liver Disease
* --- prior to procedures is not required if no oral infection is
present
Antibiotic prophylaxis
101
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
102
DRUGS - Minimize use of drugs metabolized
by liver
(4)
➢Local Anesthetic
➢Analgesics
➢Sedatives
➢Antimicrobials
103
DRUGS - Minimize use of drugs metabolized
by liver
➢Local Anesthetic
(2)
oWhy are these problematic?
oIs duration of anesthesia affected?
oAre esters better?
104
DRUGS - Minimize use of drugs metabolized by
liver
➢Analgesics
oLimit ---. recommended
maximum daily dose for an adult is ---
oHigher doses may lead to ---,
including liver failure
o--- should be avoided. Why?
oIf opioids are necessary, --- is
preferred choice- ---
oAvoid (2) -unpredictable metabolism
acetominphen (APAP)
three to four grams
toxicity
NSAIDs
hydromorphone, glucuronidation
hydrocodone, oxycodone
105
DRUGS - Minimize use of drugs metabolized
by liver
➢Sedatives
(3)
oAvoid benzodiazepines
oLorazepam –potentially used. Why?
oN2O safer, if possible
106
DRUGS - Minimize use of drugs metabolized
by liver
➢Antimicrobials
oAvoid (3) Why?
oAvoid (1). Why?
oPossible issue with ---.
Why?
oDo not drink alcohol with antibiotics
–metronidazole and 2nd and 3rd
generation cephalosporins - ---
metronidazole, tetracycline, doxycycline
azole antifungals (fluconazole)
clindamycin
Disulfiram effect
107
Caution with hypertension
➢ Portal hypertension is a complication of cirrhosis
(4)
oBP can be significantly elevated with portal hypertension
oLimit epinephrine (epi)
oDo not use retraction cord with epinephrine
othrombocytopenia (from platelet sequestration in the spleen)
108
Caution with immunosuppression
➢ Weight risk : benefit ratio
i.e., Impairment of drug metabolism : immune impairment
Patients with SEVERE LIVER DISEASE may need antibiotic prophylaxis (coverage) for
invasive/surgical procedures due to decreased immune function
