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GI > LIVER DISORDERS AND ENZYMES > Flashcards

LIVER DISORDERS AND ENZYMES Flashcards

1
Q

where does 80% of liver blood supply come from?

A

portal vein; nutrient rich

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2
Q

where does 20% of liver blood supply come from?

A

hepatic artery; oxygenated blood

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3
Q

what are liver lobes divided by?

A

coronary ligament

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4
Q

what are the functions of hepatocytes?

A
  1. remove/excrete waste, hormones, drugs, toxins-> enzymes alter substances to help urinary excretion
  2. synth plasma proteins including clotting factors-> albumin, fibrinogen, globulins
  3. produce immune factors-> phagocytes in liver produce acute phase reactants in response to microbes
  4. produce bile acid to aid in fat digestion and absorption -> excreted by liver and stored in GB
  5. excrete bilirubin -> byproduct of hGb breakdown conjugates by hepatocytes; excreted in bile
  6. store vitamins, minerals sugars-> glycogen, iron, copper, vita ADEK, B12
  7. process nutrients absorbed from digestive tract
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5
Q

how is bilirubin made?

A

catabolism of Hgb releases heme-> biliverdin-> unconjugated bilirubin-> bound to albumin or unbound

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6
Q

what is unbound bilirubin taken up by and what happens?

A

hepatocytes-> conjugated bilirubin, water-sol-> becomes part of bile

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6
Q

what is unconjugated bilirubin?

A

lipi-soluable; renal does not eliminate

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7
Q

where does bile flow into and what happens?

A

flows into common hepatic duct-> common bile-> pancreatic duct-> duodenum via sphincter of Oddi

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8
Q

where does about 50% of bile flow to?

A

into cystic duct and stored in GB

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9
Q

what is biliary obstruction?

A

blockage of bile into small intestine; inability of bilirubin to reach intestinal tract giving pale stool color

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10
Q

whats the most prevalent cause of biliary obstruction?

A

gallstones; leads to dilation of common bile duct and jaundice

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11
Q

why does jaundice occur?

A

d/t bile stasis. and buildup of conj bilirubin in blood

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12
Q

what is normal total serum bilirubin?

A

0.2-1.2

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13
Q

what levels do you see jaundice at?

A

clinically at 3

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14
Q

does normal urine contain bilirubin?

A

no

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15
Q

when will you see bilirubin in urine and what does it look like?

A

see this in obstructive jaundice; urine will have dark color

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16
Q

what is prehepatic jaundice?

A

overproduction of bile or impaired uptake by liver

AKA UNCONJ HYPERBILIRUBINEMIA

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17
Q

what is hepatic jaundice?

A

decreased conjugation

AKA UNCONJUGATED HYPERBILIRUBINEMIA

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18
Q

what is posthepatic jaundice?

A

decreased excretion (intra or extrahepatic obst.)

AKA CONJUGATED HYPERBILIRUBINEMIA

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19
Q

what do conjugated and unconjugated mean?

A

conjugated-> DIRECT
unconjugated-> INDIRECT

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20
Q

what is an increase in unconjugated bilirubin due to?

A

d/t overproduction, impairment of uptake, or impaired conjugation

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21
Q

what should you eval for when evaluating for unconjugated hyperbilirubinemia?

A

hemolytic anemia

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22
Q

what is the upper limit of normal for ALT?

A

40

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23
Q

what is the upper limit of normal for AST?

A

40

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24
Q

what is the upper limit of normal for ALK?

A

120

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25
Q

what is the upper limit of normal for GGPT?

A

51

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26
Q

what is the hallmark of hepatocellular injury?

A

elevated AST/ALT
marker of injury, inflammation, necrosis of hepatic parenchyma

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27
Q

what is the hallmark of cholestasis injury?

A

elevated alk phos +/- increased total bilirubin

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28
Q

what would a mixed pattern show?

A

both hepatocellular and cholestatic injury

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29
Q

what are the common causes of elevated liver enzymes of a hepatocellular pattern?

A

NAFLD/NASH
hep c
hep b
alcohol liver disease

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30
Q

what are the rare causes of elevated liver enzymes of a hepatocellular pattern?

A

wilsons dz
alpha 1 antitrypsin deficiency

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31
Q

what are the acute causes of elevated liver enzymes of a hepatocellular pattern?

A

meds
alcohol hepatitis
hep a
hep b

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32
Q

what are the common causes of elevated liver enzymes of a cholestatic pattern?

A

primary biliary cholangitis
primary sclerosing cholangitis
malignancy
medications

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33
Q

what liver enzymes are elevated in hepatocellular pattern?

A

AST/ALT

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33
Q

what liver enzymes are elevated in cholestatic pattern?

A

alk phos

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34
Q

what are the acute causes of elevated liver enzymes of a cholestatic pattern?

A

biliary obstruction
ABV/CMV/HSV
pregnancy

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35
Q

what are the rare causes of elevated liver enzymes of a cholestatic pattern?

A

sarcoidosis
autoimmune cholangiopathy
amyloidosis

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36
Q

what are the extrahepatic causes of elevated liver enzymes?

A

thyroid dz
muscle injury
celiac dz
chronic pancreatitis
AI
hemolysis
bone disorders
CF
right HF
malignancy
systemic infection
AIDS cholangiopathy

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37
Q

Hep A dx test

A

IgM anti HAV

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38
Q

Hep B dx test

A

IgM anti Bc
IgM anti Bs

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39
Q

Hep C dx test

A

IgM ant HCV
HCV RNA

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40
Q

autoimmune chronic liver condition dx test

A

anti smooth muscle antibody, ANA, increased GGT

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41
Q

hemochromatosis dx test

A

ferritin, Fe high. Iron infiltrates organs (pituitary, pancreas, heart)

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42
Q

wilson dz dx test

A

low ceruloplasmin, hemolysis

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43
Q

A1 antitrypsin deficiency dx test

A

low serum A1AT

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44
Q

phase 1 of hepatitis

A

viral replication
asx
labs show serologic nd enzyme markers of hepatitis

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45
Q

phase 2 of hepatitis

A

prodromal
anorexia
N/V
alterations in taste
arthralagias
malaise
fatigue
urticaria and pruritus
aversion to cig smoke
in this stage often dx w/ gastroenteritis or viral syndrome

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46
Q

phase 3 of hepatitis

A

icteric
dark urine
pale-colored stools x
GI sx and malaise
become icteric and may develop RUQ pain w/ hepatomegaly

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47
Q

phase 4 of hepatitis

A

convalescent
sx and icterus resolve
liver enzymes return to normal

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48
Q

hep a RF

A

traveling or working in countries w/ high or intermediate rates of HAV
illegal drugs (injection or not)
occupational risk exposures
close personal contact w/ international adoptee
unvax ppl in outbreaks
settings that provide service to HAV ppl

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49
Q

hep A trransmittion

A

oral fecal- overcrowding and poor sanitation
contaminated water or food- inadequately cooked shellfish

biggest RF is international travel

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50
Q

hep A incubation period

A

30 days

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51
Q

when is HAV excreted in feces

A

excreted in feces up to 2 weeks before clinical illness

52
Q

when is the greatest risk of HAV spread

A

before clinical illness occurs

53
Q

what is the cause of fulminant hep A

A

concomitant chronic hep C

54
Q

is there a chronic carrier state of HAV

A

no

55
Q

HAV clinical manifestations

A

adults-> self limited
symptomatic >70%
sx uncommon in children <6 y/o
abrupt onset fever, N/V, anorexia, abd pain, malaise
within days to weeks-> dark urine (bilirubinuria)
acholic stools
jaundice and pruritus
early s/sx diminished when jaundice appears; jaundice peaks in 2 weeks

56
Q

HAV PE

A

Jaundice, scleral icterus, hepatomegaly (80%), RUQ
tenderness to palpation.
Less common: splenomegaly and extrahepatic manifestations such
as skin rash and arthralgias.
Pregnancy: infection has been associated with increased risk of
preterm labor.
No specific disease manifestations in immunocompromised
hosts

57
Q

HAV clinical findings

A

Labs
 WBC count usually low in preicteric phase
 Mild proteinuria
 High elevations of AST and/or ALT occur early
 Hyperbilirubinemia may precede jaundice

58
Q

HAV dx

A

Detection of IgM anti-HAV antibodies. Serum IgM antibodies are detectable at the time of symptom onset, peak during the acute or early convalescent phase of the disease, and remain detectable for 3-6 months.

Detection of serum IgM antibodies in the absence of clinical symptoms may reflect prior HAV infection with prolonged persistence of IgM, a false-positive result, or asymptomatic infection (more common in children <6 years of age than in older children/adults).

Serum IgG antibodies appear early in the convalescent phase of the disease, remain detectable for decades, and are associated with lifelong protective immunity

59
Q

know course of HAV graph

A

know course of HAV graph

60
Q

HAV tx

A

Usually self-limited: supportive care.
Full clinical and biochemical recovery is observed within 3 months in 85%.
Prevention: vaccination, immune globulin, attention to hygienic practices.

61
Q

Hep B essentials of dx

A

prodrome of anorexia, N/V, malaise, aversion to smoking
fever, enlarged tender liver, jaundice
normal to low WBC count, high aminotransferase early on
liver bx-> hepatocellular necrosis and mononuclear infiltrate but is rarely indicated

62
Q

HBV etiology

A

Modes of transmission
- Inoculation of infected blood or blood products or by
sexual contact
- Present in saliva, semen, and vaginal secretions
- HBsAG-positive mothers can transmit @ delivery
- Risk of chronic infection to infant is ~90%

63
Q

HBV high risk groups

A

MSM
 IVDU
 Patients/staff at hemodialysis centers
 Physicians/PAs/Dentists/Nurses/Lab and blood bank workers

64
Q

what are most HBV cases d/t

A

heterosexual transmission

65
Q

HBV incubation period

A

Incubation period 6 weeks to 6 months

66
Q

HBV onset

A

Usually insidious in onset

67
Q

HBV aminotransferase vs HAV

A

Aminotransferase levels usually higher in HBV than in HAV

68
Q

HBV clinical findings

A

Similar to all viral hepatitis, variable
 Ranges from asymptomatic infection to fulminating disease and death in a few days
 Fever is common and low grade
 Defervescence and fall in pulse rate coincide with jaundice onset

69
Q

know HBV graph

A

ok

70
Q

HBV serology

A

HBsAg (surface antigen)
 1st evidence of infection
 Before biochemical evidence of liver disease
 Persistence >6 months signifies chronic HBV
Anti-HBs (antibody to surface antigen)
 Two sources
 Clearance of HBsAg by immune system
 Successful vaccination
 Disappearance of HBsAg and appearance of anti-HBs signals recovery, non-infectivity, and immunity
Anti-HBc
 Appears right after HBsAg
 Never appears alone
 In the setting of acute hepatitis B, IgM anti-HBc makes the diagnosis
 IgG anti-HBc persists indefinitely
 Both in recovered patients and in chronic HBV infections
HBeAg
 Secretory form of HBcAg
 Appears during incubation period after HBsAG
 Indicates viral replication and infectivity
 Persistence >3 months increases chances of chronic infection state
 Disappearance often followed by appearance of anti-HBe
 Signifies ↓ viral replication and ↓ infectivity

71
Q

HBV DNA

A

Detectable only with PCR
 Presence parallels presence of HBeAg
 HBV DNA is more sensitive and precise marker of viral replication and infectivity
 Some patients who have recovered have low level HBV DNA in liver and serum, but most are not infectious

72
Q

HBV prevention

A

 Vaccination
 Isolation from unvaccinated individuals
 Hand hygiene
 Universal precautions
 Hepatitis B immune globulin (HBIG)
 Protective/lessens severity if given within 7 days of exposure
 Followed by vaccine

73
Q

TX acute HBV

A

 Supportive as for acute hepatitis A
 Encephalopathy or severe coagulopathy indicates impending acute hepatic failure
 Transfer to liver transplant center
 Antivirals used in severe, but not mild cases
 Clinical recovery complete in 3 to 6 months
 Mortality is 0.1-1%
 Worse with superimposed Hepatitis D

74
Q

Natural HBV hx

A

Acute illness subsides over 2-3 weeks
- Clinical and laboratory recovery by 16 weeks
May become chronic
- Defined as elevated aminotransferase levels >6 months
* 40% will develop cirrhosis
* Especially if coinfected with hepatitis C and/or HIV
* Those with cirrhosis at increased risk for
hepatocellular carcinoma

75
Q

HCV >50% d/t what

A

IVDU

76
Q

HCV RF

A
  • Body piercing
  • Tattoos
  • Hemodialysis
  • Incarceration
77
Q

HCV sexual transmission

A
  • Multiple sexual partners
  • HIV coinfection
  • Unprotected receptive anal intercourse
  • Sex while high on methamphetamine
78
Q

HCV incubation period

A

Incubation period 6 – 7 weeks

79
Q

describe HCV sx

A

Clinical illness is usually mild or asymptomatic
 Jaundice more likely during acute illness
 Waxing and waning aminotransferase elevations
 >80% chance of becoming chronic

80
Q

what is aminotransferase doing in a pregnant HCV patient

A

Aminotransferases often normalize during pregnancy despite continued viremia
 Elevate again after delivery

81
Q

HCV lab findings

A

 Enzyme immunoassay (EIA) detects antibodies to HCV
 Antibodies are not protective
 Negative antibody test indicates no chronic HCV infection, no need for further evaluation.
 Other confirmatory tests
 HCV RNA measurement

82
Q

HCV graph

A

HCV graph

83
Q

HCV complications

A

 Systemic disorders:
 Membranoproliferative glomerulonephritis
 Possible relationships:
 Lichen planus
 Autoimmune thyroiditis
 Idiopathic pulmonary fibrosis
 Increased risk of non- Hodgkin lymphomas
 Insulin resistance

84
Q

HCV prevention

A

 Test donated blood
 Birth cohort screening born 1945-1965 recommended
 HCV-infected persons should practice safe sex
 Little evidence that HVC is spread easily by sexual contact or perinatally
 NO specific measures are recommended for persons in a monogamous relationship or for pregnant women
 Vaccination against HAV and HBV in patients with chronic HVC

85
Q

acute HCV tx

A

 Evolving rapidly
 Spontaneous resolution in 15% - 50%. Monitoring for spontaneous clearance for a minimum of 6 months before initiating treatment is therefore recommended.

86
Q

chronic HCV tx goals

A

 Two goals.
 Achieve sustained eradication of HCV
 Prevent progression to cirrhosis, hepatocellular carcinoma, and decompensated liver disease requiring liver transplantation.

87
Q

chronic HCV tx

A

 Antiviral therapy should be determined
on a case-by-case basis.
 However, treatment recommended for
patients with elevated serum alanine
aminotransferase (ALT) levels who meet
the following criteria:
 Older than 18 years
 Positive HCV antibody and serum
HCV RNA test results
 Compensated liver disease (eg, no
hepatic encephalopathy or ascites)
 Acceptable hematologic and
biochemical indices (hemoglobin at
least 13 for men and 12 for women;
neutrophil count >1500/mm 3, serum
creatinine < 1.5 mg/dL)
 Willingness to be treated and to
adhere to treatment requirements
 No contraindications for treatment

88
Q

TREATMENT OF HCV,
ADDITIONAL MANAGEMENT

A

 Psychologic counseling
 Alcohol avoidance
 Symptom control
 Dose adjustment of medications
 Assessment of fibrosis
 Screening for complications of cirrhosis if present

89
Q

Hep D: what is it

A

 Defective RNA virus capable of causing hepatitis in association with HBV
 Requires HBsAg
 Clears when HBsAg clears
 Can cause superinfection in patients with chronic HBV
 Fulminant hepatitis or severe chronic hepatitis that progresses rapidly to cirrhosis
 In US, new cases are infrequent because of control of HBV infection
 Immigrant population at highest risk (endemic areas, including Africa, central Asia, Eastern Europe, Amazon region of Brazil)
 Diagnosis is by detection of anti-HDV and, where available, hepatitis D antigen
(HDAg) or HDV RNA in serum.

90
Q

Hep E: what is it

A

 Major cause of acute hepatitis throughout Central and Southeast Asia, the Middle East, and North Africa
 Consider in those traveling to endemic areas
 In industrialized countries, may be spread by swine; having pet in the home and consuming undercooked organ meats or infected cow’s milk are risk factors.
 Risk increased in patients undergoing hemodialysis.
 In endemic areas, mortality rate is high in pregnant women.
 Generally is self-limited, no carrier state. Risk of hepatic decompensation and death increased if underlying chronic liver disease.
 Problematic in transplant situation

91
Q

dx Hep E test

A

Diagnosis by testing for IgM anti-HEV in serum, although available tests may not be reliable.
A 3-month course of treatment with oral ribavirin has been reported to induce sustained clearance of HEV RNA in patients with persistent HEV infection and may be considered in patients with severe acute hepatitis E

92
Q

NAFLD (NONALCOHOLIC FATTY LIVER DISEASE) main contributing factors

A
  • Obesity
  • Diabetes mellitus
  • Hypertriglyceridemia
  • Risk 4 to 11 x higher in those with metabolic syndrome/insulin resistance
  • Physical activity may be protective
93
Q

what is caput medusae

A

One of the cardinal features of portal hypertension. The appearance is due to cutanous portosystemic collateral formation between distended and engorged paraumbilical veins that radiate from the umbilicus across the abdomen to join systemic veins.

94
Q

NAFLD CLINICAL
SIGNS/SYMPTOMS

A
  • Asymptomatic or mild RUQ discomfort
  • Hepatomegaly ~75%
  • May or may not be stigmata of chronic liver disease
  • Signs of portal hypertension if advanced fibrosis/cirrhosis
  • NAFLD Fibrosis Score (http://nafldscore.com)
95
Q

NAFLD LAB FINDINGS

A

 May be mild or moderate elevations in AST and ALT.
 Degree of aminotransferase elevation does not predict degree of hepatic inflammation or fibrosis
 Normal levels do not exclude NAFLD.
 When elevated, AST and ALT typically 2x to 5x upper limit of normal, with AST/ALT ratio of <1 (unlike alcoholic fatty liver disease, which typically has AST/ALT ratio >2).
 Alkaline phosphatase may be elevated to 2x to 3x upper limit of normal.
 Serum albumin and bilirubin levels are typically within the normal range.
 May be elevated serum ferritin or transferrin saturation.

96
Q

NAFLD IMAGING

A

 US: hyperechoic texture/bright liver because of diffuse fatty infiltration.
 Biliary dilatation suggests extrahepatic cholestasis due to gallstones, strictures, or malignancy. Absence of biliary dilatation suggests intrahepatic cholestasis.
 CT and MRI can identify steatosis but not inflammation or fibrosis.
 Magnetic resonance spectroscopy (MRS) is quantitative, but not widely available.
 Study compared MRS with liver biopsy: correlation between measurement of intrahepatocellular lipid by MRS and histologic assessment of cirrhosis.

97
Q

NAFLD DIAGNOSIS

A

 Requires all of these:
 Hepatic steatosis by imaging or bx
 Exclusion of significant alcohol consumption
 Exclusion of other causes of hepatic steatosis
 Absence of coexisting chronic liver disease
 Radiologic findings can make diagnosis if other causes of hepatic steatosis have been excluded.
 Liver biopsy if diagnosis not clear or to assess degree of hepatic injury.
 Bx is only method to differentiate NAFLD from NASH.

98
Q

NAFLD TREATMENT

A

 Lifestyle changes
 Drugs
 Vitamin E, 800 U?
 Metformin (may not improve liver histology)
 TZDs, GLP-1
 Liver transplant
 For advanced cirrhosis

99
Q

CIRRHOSIS ESSENTIALS OF DX

A

 Result of injury that leads to both fibrosis and regenerative nodules.
 May be reversible if cause is removed.
 The clinical features result from hepatic cell dysfunction, portosystemic shunting, and portal hypertension

100
Q

CIRRHOSIS ETIOLOGIES

A

 Most common:
 Chronic alcoholism
 Chronic viral hepatitis (B/C)
 Hemochromatosis
 NAFLD/NASH

101
Q

LESS COMMON ETIOLOGIES OF CIRRHOSIS

A

 Autoimmune hepatitis
 Primary and secondary biliary cirrhosis
 Primary sclerosing cholangitis
 Medications (methotrexate, isoniazid)
 Wilson disease
 Alpha-1 antitrypsin deficiency
 Celiac disease

102
Q

CIRRHOSIS S/SX

A

 Hepatocyte dysfunction
 Inability of hepatocyte to
perform normal tasks
 Portosystemic shunting
 Portal vein blood flow not
flowing through liver
 Blood not presented to
hepatocytes for processing
 Portal hypertension
 Portal system, like pulmonary
system, is low pressure
 Obstructed liver blood flow
results in “back pressure”

103
Q

CIRRHOSIS CLINICAL
MANIFESTATIONS

A

 May have no symptoms for long periods.
 Symptom onset usually insidious.
 Fatigue, disturbed sleep, muscle cramps, weight loss are common.
 Advanced cirrhosis:, anorexia may be extreme, with associated N/V, reduced muscle strength/exercise capacity.
 May be abdominal pain.
 Menstrual abnormalities (amenorrhea), erectile dysfunction, loss of libido, gynecomastia
 Hematemesis is presenting symptom in 15–25%

104
Q

COMPLICATIONS OF PORTAL
HYPERTENSION

A

 Esophageal varices
- Hematemesis
 Gastric varices
- Melena
 Splenomegaly
- Dilated abdominal veins
 Rectal varices
- Hemorrhoids
 Ascites
- Increased hydrostatic pressure

 Hepatic encephalopathy
 Accumulation of serum ammonia in the brain due to lack of excretion by liver
 Precipitating Factors: infection, GI bleeding,
hyponatremia, hypovolemia, sedating drugs
 Clinical Findings: decreased mental function, poor
concentration, Asterixis, stupor
 Diagnosis: no gold standard
 Clinical findings/psychometric testing
 Serum ammonia levels not useful
 Management:
 Non-absorbable disaccharides: Lactulose
 Non- absorbable antibiotics: Rifaxamin (suppresses
bowel flora, decreasing ammonia production)

105
Q

TX OF HEPATIC ENCEPHALOPATHY : LACTULOSE

A

 Non-absorbable disaccharide syrup
 Digested by colonic bacteria
 Acidifies colon contents
 Favors formation of non-absorbable
ammonium ion (NH4+)
 Favors change in bowel flora: fewer
ammonia-forming organisms
 Continued use after acute episode may
reduce frequency of recurrences

106
Q

extrahepatic complications of portal HTN/cirrhosis

A

 Hepatorenal Syndrome
 Deterioration of kidney function
due to alterations in blood flow
 High mortality rate
 Liver transplant definitive therapy
 Hepatopulmonary Syndrome
 Hypoxemia secondary to vasodilation in lungs
 Symptoms: Platypnea-orthodeoxia (dyspnea and deoxygenation when changing from a recumbent to an upright position)
 Management: Supplemental O2, liver transplant

107
Q

complications of cirrhosis

A

 Bleeding from varices
 Hepatic failure
 Increased risk of hepatic cancer
 Increased risk of infection/sepsis

108
Q

acute liver failure: what is it

A

Rapid development of hepatocellular dysfunction with
associated coagulopathy and mental status changes in patient without known prior liver disease

109
Q

acute liver failure: causes

A
  • Medications: most common in US is acetaminophen
  • Alcohol
  • viral Hepatitis
  • Acute fatty liver of pregnancy
  • Wilson disease
  • Autoimmune hepatitis
110
Q

acute liver failure: sx

A
  • Confusion, jaundice, ascites
  • High mortality
111
Q

acute liver failure: dx

A

 History = hepatic encephalopathy
 Blood work: elevated transaminases (often with abnormal bilirubin and alk phos); prolonged prothrombin time (INR ≥1.5)
 CT head

112
Q

acute liver failure: tx

A

 ICU monitoring
 Supportive treatment: fluid balance, mechanical
ventilation, treatment of underlying cause
 Liver transplant if no improvement

113
Q

cirrhosis labs

A

 May be normal in early disease
 Alcohol suppresses marrow production of all cell
lines.
 Thrombocytopenia, most common cytopenia, due to
sepsis, folate deficiency, or splenic sequestration.
 Anemia, frequent, often macrocytic
 Causes include folate deficiency, hemolysis,
hypersplenism, occult/overt GI blood loss
 WBC may be low, reflecting hypersplenism, or high
suggesting infection.
 Prolonged PT from reduced levels of clotting factors.
 Abnormalities of fibrinolysis: increased risk of venous thromboembolism.
 Hepatocellular injury/dysfunction:
modest elevations of AST and alkaline
phosphatase, progressive elevation of bilirubin.
 Serum albumin decreases as disease
progresses; gamma-globulin levels are increased.
 Risk of DM increased, esp when HCV
infection, alcoholism, hemochromatosis, NAFLD.
 Vitamin D deficiency common.

114
Q

imaging in cirrhosis

A

 US
 Assess liver size
 Detect ascites
 Detect hepatic nodules
 Combined with Doppler may establish patency of splenic, portal, and hepatic veins
 Contrast-enhanced CT good for characterizing nodules
 CT or ultrasound guided biopsy if malignancy is suspected

115
Q

other tests

A

 Esophagogastroduodenoscopy (EGD)
 Confirms presence of varices
 Detects specific causes of bleeding

116
Q

liver biopsy

A

GOLD STANDARD FOR DX
FibroTest (FibroSure in the US):
biomarker test that uses six blood
serum tests to generate a score
correlated with degree of liver damage.
May eventually have same prognostic
value as liver biopsy

117
Q

cirrhosis tx

A

 Review treatment of esophageal varices
 Abstinence from alcohol.
 Palatable diet, with adequate calories and protein and, if fluid retention, sodium restriction.
 In hepatic encephalopathy, protein intake should be reduced to no less than 60–80 g/day.
 Vitamin supplementation.
 HAV, HBV, pneumococcal vaccines, yearly influenza vaccine, COVID vaccine.

118
Q

ascites: what is it

A

 Results from portal hypertension:
 With increased hydrostatic pressure, this results in hypoalbuminemia, decreasing oncotic pressure.
 Peripheral vasodilatation, impaired hepatic inactivation of aldosterone; and increased aldosterone secretion secondary to increased renin production.

119
Q

tx cirrhosis/ascites

A

 Diagnostic paracentesis for ascites
 Cell count and culture, ascitic albumin level (serum albumin minus ascitic fluid albumin ≥ 1.1suggests portal hypertension).

120
Q

liver transplant

A

 Evaluation should be considered once a patient with cirrhosis has experienced a complication such as ascites, hepatic encephalopathy, or variceal hemorrhage or hepatocellular dysfunction
 Comprehensive medical, surgical and psychiatric evaluation
 Cardiac, pulmonary, dental, cancer screening
 Transplant priority based on severity of hepatic dysfunction based on MELD-Na
(Model of End Stage Liver Disease score) https://www.mdcalc.com/meldna-meld-na-score-liver-cirrhosis
 Exclusion criteria include: severe pulmonary HTN, extrahepatic malignancy, severe
cardiopulmonary disease, severe vascular disease, uncontrolled infection, active
substance abuse, lack of adequate social support, poorly controlled psychiatric illness

121
Q

assessment of liver fxn

A

 CTP score is obtained by
adding the score for each
parameter
 CTP class:
 A = 5-6 points
 (100% survival)
 B = 7-9 points
 (80% survival)
 C = 10-15 points
 (45% survival)

122
Q

alcohol liver disease

A

Major cause of liver disease in United States
 15-20% chronic heavy drinkers develop hepatitis or cirrhosis
 Defined as 60-80 g/day for men and 20g/day for women
Risk Factors
* FHx, Hx substance abuse, underlying depression or anxiety disorder
Signs and Symptoms
* Acute hepatitis can present with signs of liver failure: jaundice, ascites, etc.
Diagnosis
* History, history, history**
* 2:1 ratio of AST/ALT
* Serum alcohol level, ethyl gluconuride
* Iron Studies ( ferritin, iron, TIBC), Folate, Vitamin B12
* Liver biopsy not warranted
Treatment
* Abstinence and counseling
* Steroid taper in acute alcoholic hepatitis?

123
Q

budd-chiari syndrome

A

 Syndrome in which a clot causes narrowing or blockage of the hepatic veins
 Primary venous process vs. Secondary compression process
 Risk Factors
 Hypercoagulable state – pregnancy, oral contraception, sickle cell disease, polycythemia, etc.
 Signs and Symptoms
 Acute vs. chronic blockage
 RUQ pain, fatigue, tenderness, abdomen fullness,
jaundice, ascites/ lower extremity edema
 Diagnosis
 Ultrasound with doppler is gold standard
 CT/MRI/Venography
 Treatment
 Correcting underlying disorders
 Anticoagulation
 Angioplasty/liver transplant for those who have
progressed

124
Q

primary biliary cirrhosis

A

 Small intrahepatic bile ducts
 Labs: ALK > > AST/ALT; Anti mitochondrial Antibody (AMA) +
 Common in woman
 Dx: US evaluation to rule out obstruction; Liver Biopsy to confirm Dx if AMA
 Sx: itching, sjogren’s syndrome, fatigue
 Treatment: Ursodeoxycholic acid (UDCA)

125
Q

autoimmune hepatitis

A

 Labs:
 AST/ALT&raquo_space; ALK Phos
 Antinuclear Antibody (ANA) +
 Elevated Gamma Globulins (IgG)
 Anti-smooth Muscle antibody (SMA) +
 More common in woman
 Dx: Liver biopsy to confirm Dx
 Sx: fatigue/flu-like
 Can present as fulminant hepatic failure
 Treatment includes Prednisone taper and Azathioprine

126
Q

primary sclerosing cholangitis

A

 Leads to narrowing of intra- and extrahepatic bile ducts
 Labs: Alk phos = ALT/AST, Elevated Total Bilirubin
 Association with Ulcerative Colitis
 Sx: jaundice, itching
 Risk of cholangitis
 Tx: MRCP/ERCP with stenting
 Increased risk for Cholangiocarcinoma

127
Q

metabolic disorders

A

Hemochromatosis
*Iron Overload leading to iron accumulation within liver
*Patients of northern European descent
*Labs: Iron/ferritin/TIBC if clinical suspicion, If iron
saturation >45%, check genetic testin
*Dx: Liver biopsy with hepatic iron index, Imaging: MRI
*Treatment includes phlebotomy or iron chelation therapy
Alpha 1 Antitrypsin Deficiency
*Genetic disorder leading to defective production of A1AT
*Can affect lungs and liver, Suspect with early onset
COPD
*Labs: Serum A1AT level, A1AT phenotype
*Tx: A1AT infusion for lung related disease, Supportive
care/transplant for liver related disease
Wilson Disease
*Autosomal recessive disorder related to ineffective copper metabolism
*Young patients with neuropsychiatric symptoms
*Labs: Serum ceruloplasmin, 24 hour urine copper
*Dx: Slit lamp exam for Kayser- fleischer rings
*Management includes genetic counseling and copper
chelation

128
Q

clinical pearls

A

 AST/ALT are associated with hepatic inflammation, not hepatic synthetic function.
INR, albumin, and bilirubin are associated with hepatic synthetic function
 To confirm hepatitis C with active viremia, one must have a positive Hepatitis C RNA
 Presence of Positive HBV surface Ab in absence of other positive markers is consistent with immunization
 Thrombocytopenia can indicate cirrhosis with portal hypertension (sequestration of platelets in enlarged spleen)
 Screen all patients with advanced fibrosis/cirrhosis for cancer

GI (22 decks)

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