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Dental Management of a Complex Patient > Gastrointestinal and Hepatic Disease Part 1 > Flashcards

Gastrointestinal and Hepatic Disease Part 1 Flashcards

1
Q

Liver

A
  • Largest internal organ; located in the R upper quadrant
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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

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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

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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

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5
Q

Hepatic Veins –

A

drain venous blood from liver to inferior vena cava and on to the right

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6
Q

Hepatic Artery –

A

provides oxygen and nutrition to liver tissues

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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

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8
Q

Function of hepatocytes
➢ Synthesizes proteins
(6)

A
  • Immunoglobulins
  • Albumin
  • coagulation factors
  • carrier proteins
  • growth factors
  • hormones
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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

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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.

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11
Q

➢ Increased bilirubin – (5)

A

jaundice,
fatigue,
cutaneous itch,
discolored urine,
discolored feces (?)

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12
Q

Function of hepatocytes
➢ Regulates nutrients
(4)

A
  • glucose
  • glycogen
  • lipids
  • amino acids
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13
Q

Function of hepatocytes
➢ Regulates –
➢ Prepares drugs for –
➢ Responsible for (2)

A

nutrients
excretion
drug conjugation and metabolism

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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.)

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15
Q

Types of damage
(5)

A

➢ Hepatocellular (inflammation and injury)
➢ Cholestatic (obstructive)
➢ Mixed
➢ Cirrhosis (fibrotic, end-stage); acute or chronic
➢ Neoplastic

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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

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17
Q

Signs

A

➢ Jaundice
➢ Ascites
➢ Edema
➢ GI bleed
➢ Dark urine
➢ Light stool
➢ Mental confusion
➢ Xanthelasma
➢ Spider angiomas
➢ Palmar erythema
➢ Asterixis
➢ Hyperpigmentation

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18
Q

Symptoms

A

➢ Appetite loss ֎
➢ Bloating
➢ Nausea
➢ RUQ pain
➢ Fatigue
➢ Mental confusion

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19
Q

Asterixis
(3)

A
  • a.k.a. flapping tremor
  • classic sign in hepatic encephalopathy (HE)
  • jerky movements when hands are extended at wrists.
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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

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21
Q

HE can be a chronic problem in patients with

A

cirrhosis, managed medically to varying degrees of success, punctuated with occasional exacerbations

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22
Q

although these acute exacerbations of HE are rarely fatal, they are a frequent cause of

A

hospitalizations among patients with cirrhosis

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23
Q

Blood Tests
(2)

A

*Complete Blood Count (CBC)
*Comprehensive Metabolic Panel (CMP)

Multiple others available for specific patient evaluations

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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
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25
Q

Multiple others available for specific patient evaluations
(6)

A
    • lipid panel
    • VDRL
    • PSA (prostate specific antigen)
    • SARS Ag, SARS Ab, HIV, Hep B, etc.
    • bleeding times
    • et cetera
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26
Q

evaluate the cells that circulate in blood
(3)

A

red blood cells (RBCs)
white blood cells (WBCs)
platelets (PLTs)

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27
Q

may detect a variety of diseases and conditions
(5)

A
  • infection
  • anemia
  • leukemia
  • lymphoma
  • neutropenia
  • etc.
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28
Q

Comprehensive Metabolic Panel (CMP)
(3)

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
  • there are also SMAC 8, 12, 16 and 20 variants
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29
Q

Comprehensive Metabolic Panel (CMP)
Includes
(5)

A
  • General tests
  • Kidney function assessment
  • Electrolytes
  • Protein tests
  • Liver function assessment
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30
Q

Liver Function Tests
(5)

A

*Bilirubin
*Alkaline phosphatase (ALP)
*Transaminases
*Albumin
*Globulin

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31
Q

Transaminases
(3)

A
  • Aspartate amino transferase (AST or SGOT)
  • Alanine amino transferase (ALT or SGPT)
  • Gama-Glutamyl Transferase (GGT)
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32
Q

Liver Function Test
➢ Bilirubin (high)
(2)

A

oProduct of heme breakdown
oIncreased total bilirubin, increased severity of liver injury

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33
Q

Unconjugated (indirect)
(3)

A

❖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)

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34
Q

Conjugated bilirubin (direct)
(3)

A

❖Increased SERUM indicative of liver disease
❖Water-soluble, excreted by kidney
❖All URINE bilirubin is conjugated

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35
Q

Alkaline phosphatase (high)
(3)

A

oaltered in myriad of diseases especially bone neoplasms
onot specific to liver disease,
omay indicate cholestatic disease

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36
Q
  1. AST - Aspartate Aminotransferase (SGOT)
A

–a.k.a. Serum Glutamic-Oxaloacetic Transaminase-
–related to glutamic oxalate metabolic pathways

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37
Q
  1. ALT - Alanine Aminotransferase (SGPT)
A

–a.k.a. Serum Glutamic-Pyruvic Transaminase-
–part of pyruvate pathway in cell metabolism

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38
Q
  1. Gama-Glutamyl Transferase (GGT)
    - needed for — synthesis
    - useful to detect —
    - can detect the slightest degree of —
    - sensitive to (3)
    - good marker for(3)
A

protein
alcohol-induced liver cell injury and chronic alcoholics
cholestasis
biliary obstruction, cholangitis, and cholecystitis
pancreatic cancer, prostatic carcinoma, and liver cell carcinoma

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39
Q

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)

A

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

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40
Q

Liver Function Test
➢ Albumin (low)
(3)

A

oSynthesized “exclusively by hepatocytes”
oHalf-life: 18-20 days
oHypoalbuminemia

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41
Q

oHypoalbuminemia
(2)

A

❖More indicative of chronic liver disease
❖Not specific to liver disease
✓ Malnutrition
✓ Chronic infection
✓ Gut disease

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42
Q

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 —

A

VIII (vascular endothelial cells)
I, II, V, VII, X
II, VII, IX, X
PT-INR

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43
Q

All viral hepatitis are RNA virus, except for

A

Hep B (HBV) which is
enveloped DNA virus

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44
Q

Hepatocellular damage –> host immune response to viral antigens rather
than direct cytopathic effect from virus
(4)

A

oCytotoxic T-cells
oProinflammatory cytokines
oNatural killer cell response
oAntibody-dependent cellular cytotoxicity

45
Q

Infection may be asymptomatic/symptomatic and acute/chronic
(4)

A

oPatient may clear the virus or virus may become inactive
oReactivation may occur
oChronic hepatitis can lead to
oWhen chronic infection but asymptomatic

46
Q

Chronic hepatitis can lead to
(4)

A

❖ Cirrhosis
❖ Liver failure
❖ Hepatocellular carcinoma.\
❖ Risk factor for immunosuppression

47
Q

When chronic infection but asymptomatic
(1)

A

❖ Carrier state (low levels)

48
Q

Viral Hepatitis
(4)

A
  • Serum hepatitis, blood-borne
  • Parenteral, intimate and sexual exposure
  • Populations at risk?
  • Coinfection?
49
Q

Hepatitis B (Hep B; HBV)
➢ Virus can last for up to – days on an infected surface
➢ Incubation period: – days average
➢ Reactivation
➢ Peg-

A

7
90
interferon or antivirals such as entecavir and tenofovir

50
Q

HBV
➢ Chronicity:
–% for infants
–% in children (1-5)
–% in adults

A

o90
o25-50
o<5

51
Q

Vaccination
(2)

A

o3 doses (initial, 1 month, 6 months)
oSeroconversion necessary - What does this mean?

52
Q

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 =

A

53%
Baby boomers
15-25
chronic (75-85%)
needlestick
vaccine
undetectable HCV RNA levels after 12 weeks of recommended protease
inhibitor therapy

53
Q

➢ Has high risk for becoming chronic (75-85%)
(3)

A

o10-20% develop cirrhosis (takes 20-30 years)
oIncreased risk for hepatocellular carcinoma (HCC)
oIncreased risk of death

54
Q

➢ Cure = undetectable HCV RNA levels after 12 weeks of recommended protease
inhibitor therapy
(3)

A

oMavyret (glecaprevir/pibrentasvir)
oEpclusa (sofosbuvir/velpatasvir)
oHarvoni (ledipasvir/sofosbuvir)

55
Q

Hepatitis D (Hep D; HDV)
(3)

A

➢ Usually coinfection with HBV
➢ More severe than HBV alone
➢ Higher risk of fulminant hepatitis
oMassive hepatocellular destruction

56
Q

Hepatitis A and E
(3)

A

➢ Infectious hepatitis, fecal-oral transmission
➢ Highly contagious and transmissible
➢ Vaccination available for HAV

57
Q

Viral Hepatitis Considerations
* Most carriers of (3) are unaware they have hepatitis
* Hepatitis can be contracted by
* Chronic, active, hepatitis patients may have

A

HBV, HCV, HDV
the dentist from an infected patient
chronic liver dysfunction

58
Q

Chronic, active, hepatitis patients may have chronic liver dysfunction
(2)

A

➢ Increased bleeding
➢ Altered drug metabolism

59
Q

Hep — is most likely viral hepatitis to be transmitted occupationally to a dental
health care worker, followed by Hep

A

B
C

60
Q

Little to no risk exists for transmission of

A

HAV, HEV, and non-A-E hepatitis viruses

61
Q

Reduce oral healthcare worker infection by:
(2)

A

➢ ALL patients considered infectious standard (universal) precautions
➢ HBV vaccination

62
Q

in the 1990s with public attention to higher population incidences of Hep B, dentists
(and other healthcare workers at risk)

A

got the vaccine (3 doses (initial, 1 month, 6
months); then 5 - 10 years later, the HBIg booster was recommended

63
Q

Most youth get the vaccine today, so there is less public concern;
but

A

standard (universal) precautions universal precautions have helped control this
risk

64
Q

Viral Hepatitis Considerations
* Determine
(2)

A

➢ Circumstances of infection (age at onset, source of infection)
➢ Status of viral hepatitis
oSerology
oHow/if treated
oViral load

65
Q

Consider screening for patients in high-risk categories
(4)

A

➢ Hep B
➢ Hep C
➢ HIV
➢ Other STDs (HIV, syphilis, gonorrhea, etc.)

66
Q

Patients with active hepatitis (acute or chronic)
(2)

A

➢ 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
Q

Patients with history of hepatitis (resolved, chronic inactive)
(2)

A

➢ Consider risk factors
➢ Consult physician to determine liver status

68
Q

Needlestick
(2)

A

➢ Consult the physician
➢ Consider hepatitis B immunoglobulin →Why? What kind of immunity?

69
Q

Viral Hepatitis Oral Manifestations
(5)

A
  • Bleeding
  • Mucosal jaundice
  • Glossitis
  • Angular cheilosis
  • Extrahepatic immunologic disorders with chronic HCV
    ➢ Oral lichen planus
    ➢ Lymphocytic sialadenitis (Sjögren-like syndrome)
70
Q

Drug-Induced Liver Disease
* May be a cause as well as consequence of
* Myriad of drugs may cause

A

liver disease
liver disease (e.g. APAP, clindamycin, etc.)

71
Q

Drug-Induced Liver Disease
Mechanisms
(3)

A

➢ Direct toxicity to hepatocytes
➢ Production of hepatotoxic metabolites
➢ Accumulation of drug due to altered metabolism

72
Q

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

A

hepatotoxic
inflammation
10

73
Q

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,

A

fatty liver –reversible
irreversible changes
and necrosis
fibrosis and cirrhosis develop –irreversible -
leading to hepatic failure

74
Q

Alcoholic Liver Disease
Complications
(6)

A

➢ Bleeding tendencies –alcohol can impair platelet function
➢ Unpredictable drug metabolism
➢ Potential impaired immune function
➢ Peripheral neuropathies
➢ Dementia and psychosis
➢ Anorexia

75
Q

Alcoholic Liver Disease
* Complications of cirrhosis
(5)

A

➢ Ascites –hepatorenal syndrome
➢ Esophageal varices –GI bleed
➢ Jaundice
➢ Hepatosplenomegaly
➢ Coagulation disorders

76
Q

Hepatosplenomegaly
(3)

A

oEnlarged spleen due to portal hypertension
oDecreased platelet function
oLeads to thrombocytopenia

77
Q

Coagulation disorders
(3)

A

oDecreased synthesis of clotting factors
oImpaired clearance of anticoagulants
oDecreased vitamin K absorption (requires biliary excretion)

78
Q

Complications of cirrhosis
(4)

A

➢ Hypoalbuminemia
➢ Anemia
➢ Neutropenia
➢ Encephalopathy –neurotoxins not removed from liver

79
Q

➢ Anemia
(2)

A

oIron deficiency
oMacrocytosis

80
Q

Alcoholic Liver Disease
* Identify alcoholic patients via
(5)

A

➢ History
➢ Clinical examination
➢ Detection of odor on breath
➢ Suspicious behavior
➢ Information from family/friend

81
Q

Consult physician to determine the status of liver dysfunction
➢ Early on/mild dysfunction:
➢ Severe liver dysfunction,

A

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
Q

Alcoholic Liver Disease Considerations
* Patients with, suspected, active, untreated alcoholic liver disease are not
candidates for

A

routine, elective dental treatment
➢ Refer to physician for treatment

83
Q

Oral neglect is common in those who

A

abuse alcohol
➢ Pts should demonstrate interest and the ability to care for their dentition before
any significant treatment is provided

84
Q
  • AST:ALT ratio ≥— and elevated GGT are suggestive of alcoholic liver disease
A

2

85
Q
  • Maintain good hygiene to avoid
A

spreading of infection given reduced immune
capabilities with advanced liver disease whether alcoholic or not.

86
Q

Alcoholic Liver Disease Oral Manifestations

A
  • Neglect
  • Bleeding
  • Ecchymoses
  • Petechiae
  • Glossitis
  • Angular cheilosis
  • Alcohol odor
  • Parotid enlargement
  • Xerostomia
87
Q
  • A patient with jaundiced mucosal
    tissues and breath that is
A

sweet and
musty is associated with liver
failure.

88
Q
  • Alcohol abuse is a strong risk factor
    for
A

oral squamous cell carcinoma

89
Q

*— is the number one abused drug in terms of emergency room visits, hospital
admission, family violence, and other social problems

A

Alcohol Abuse

90
Q

General Dental Treatment Considerations in Liver Disease
* Laboratory tests may be needed to evaluate the fitness of the patient for dental
treatment(s)
(2)

A

➢ Complete blood count with differential
➢ Liver function test which includes:

91
Q

➢ Complete blood count with differential

A

oPlatelet count is included in a routine CBC

92
Q

Liver function test which includes:
(6)

A

oAST
oALT
oGGT
oAlbumin
oAlkaline Phosphatase
oBilirubin

93
Q

Laboratory tests may be needed to evaluate the fitness of the patient for dental
treatment(s)
➢ Bleeding studies
(2)

A

oPT (PT-INR)
oBleeding time

94
Q

Active liver disease:
(3)

A

➢ 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
Q

History of liver disease
(4)

A

➢ Age at onset
➢ Consult physician to determine status and medication usage
➢ Compensated disease or decompensated disease
➢ Assess other end-organ damage

96
Q

Assess other end-organ damage
(4)

A

oGall bladder
oRenal
oCardiovascular
oHematologic disease (anemia, bleeding and prothrombotic states –failure to clear
coagulation factors –risk for Disseminated Intravascular Coagulation (DIC)

97
Q

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)

A

physician
decompensated
medications
anticoagulants
labs

❖ Vitamin K
❖ Fresh frozen plasma (contains all coagulation factors)
❖ Platelet transfusion

98
Q

➢ PERI/INTRA
oPerform — as atraumatically as possible
oIf performing a scaling and root planing, do —
oHave — available

A

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
Q

➢ 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

A

20
NSAIDs
acetaminophen
gauze
clot in place (no straws, no spitting, avoid
talking and maintain soft diet for 2-3 days)
bleeding

100
Q

General Dental Treatment Considerations in Liver Disease
* — prior to procedures is not required if no oral infection is
present

A

Antibiotic prophylaxis

101
Q

Patients with SEVERE LIVER DISEASE may need antibiotic prophylaxis (coverage)
for

A

invasive/surgical procedures due to decreased immune function
➢ Weight risk/benefit ratio
Impairment of drug metabolism vs immune impairment

102
Q

DRUGS - Minimize use of drugs metabolized
by liver
(4)

A

➢Local Anesthetic
➢Analgesics
➢Sedatives
➢Antimicrobials

103
Q

DRUGS - Minimize use of drugs metabolized
by liver
➢Local Anesthetic
(2)

A

oWhy are these problematic?
oIs duration of anesthesia affected?
oAre esters better?

104
Q

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

A

acetominphen (APAP)
three to four grams
toxicity
NSAIDs
hydromorphone, glucuronidation
hydrocodone, oxycodone

105
Q

DRUGS - Minimize use of drugs metabolized
by liver
➢Sedatives
(3)

A

oAvoid benzodiazepines
oLorazepam –potentially used. Why?
oN2O safer, if possible

106
Q

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 - —

A

metronidazole, tetracycline, doxycycline
azole antifungals (fluconazole)
clindamycin
Disulfiram effect

107
Q

Caution with hypertension
➢ Portal hypertension is a complication of cirrhosis
(4)

A

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
Q

Caution with immunosuppression

A

➢ 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

Dental Management of a Complex Patient (13 decks)

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