Liver Flashcards
(138 cards)
1
Q
AST:ALT >2 means
A
alcoholic hepatitis
SSSSSIpping
2
Q
ALT>AST means
A
viral/toxic/inflammatory processes
3
Q
AST and ALT > 1000 means
A
acute viral hepatitis (A and B mostly)
4
Q
increased ALP + GGT suggests
A
hepatic source or biliary obstruction
5
Q
Increased ALT, + ANA, and + smooth muscle antibodies
responding to steroids
means
A
autoimmune hepatitis
6
Q
which acute hepatic illnesses are associated with chronicity?
A
HBV, HCV, HDV
7
Q
Fatigue, weakness, sleep disturbance, anorexia, unintentional weight loss, N/V
RUQ pain, vague abdominal discomfort
Pruritus, jaundice, bleeding
PE: muscle wasting, spider telangiectasias, petechiae/ecchymoses, palmar erythema, caput medusae, hepatomegaly, nodular liver edge, splenomegaly, dupuytren contractures, edema, delirium, AMS, asterixis
Enlarged abdomen with small extremities (ascites), gynecomastia
A
cirrhosis
8
Q
RF for —:
Cholestatic disease
Autoimmune disease
Metabolic disease
Hepatic biliary obstructive disease
Hepatic venous outflow obstruction (RHF)
A
cirrhosis
9
Q
Diffuse fibrosis of the liver, secondary to ongoing, chronic liver injury
Loss of normal structure of the liver due to scarring and “regenerative nodules” → loss of function
Irreversible → compensated or decompensated phases
Downstream complications related to ½ root causes:
Synthetic dysfunction (liver insufficiency)
Dysregulated circulatory dynamics (portal HTN)
Alcoholic liver disease, chronic hepatitis C, NAFLD, NASH (metabolic syndrome), chronic hepatitis B
A
cirrhosis
10
Q
What are the two types of cirrhosis?
A
compensated and decompensated
11
Q
Consider in anyone with chronic liver disease
Compensated = may not be detectable, hinging on liver biopsy/histology “gold standard” —
Labs: increased INR, bilirubin, low albumin
Thrombocytopenia most sensitive and specific
Imaging: US/CT/MRI: enlarged liver, splenomegaly, collateral vessels
Decompensated = complications in setting of chronic liver disease is essentially diagnostic
varices/hemorrhage
Ascites
Hyponatremia
Portal venous thrombosis
Encephalopathy
jaundice
A
cirrhosis
12
Q
What signs indicate decompensated cirrhosis?
A
varices/hemorrhage
Ascites
Hyponatremia
Portal venous thrombosis
Encephalopathy
jaundice
13
Q
— is the most sensitive and specific for cirrhosis
A
thrombocytopenia
14
Q
what is gold standard for cirrhosis?
A
liver biopsy
15
Q
MELD-Na score → 3 month mortality risk
Bilirubin
Cr
Na+ level
INR
>17 = liver transplant
Child-Pugh class → 1 year survival rate, likelihood of developing complications
Bilirubin
Albumin
PT
Ascites, encephalopathy
Class A = 100%, B = 80%, C = 45%
A
cirrhosis
16
Q
how do you treat cirrhosis?
A
Ascites + edema: sodium restriction, diuretics
Pruritus: cholestyramine
US every 6 months
17
Q
Prodrome of anorexia, nausea, vomiting, malaise, aversion to smoking, URI symptoms
Spiking fever, enlarged and tender liver, jaundice (after 5-10 days)
Abdominal pain mild and constant in RUQ or epigastric aggravated by jarring or exertion
After 5-10 days = dark urine, pale, acholic stools → jaundice, icteric sclera, pruritus
A
acute hepatitis A
18
Q
crowding and poor sanitation, and international travel are RF for
A
acute hep A
19
Q
hep A is spread through
A
Fecal-oral route - person-person, or ingestion of contaminated food/water w/ incubation ~30 days
20
Q
LABS: Normal-low WBC
Markedly elevated aminotransferases
Bilirubinuria
Strikingly elevated AST or ALT early (ALT>AST) → bilirubin/ALP elevation
anti-HAV +
PE: Hepatosplenomegaly, RUQ tenderness to palpation, jaundice
IgM anti-HAV only for symptomatic persons
Past exposure = IgG HAV Ab with negative IgM
A
acute hep A
21
Q
how do you treat acute hep A
A
Bed rest
N/V → IV glucose
Avoid strenuous exertion, alcohol, hepatotoxic agents
22
Q
does Hep A have risk of chronic liver disease?
A
no
23
Q
Onset abrupt or insidious with low grade fever, fall in pulse rate w/ jaundice, anorexia, malaise, N/V, aversion to smoking
Dark urine, pale, acholic stools, jaundice + pruritus
A
acute hep B
24
Q
acute hep B is associated with
A
glomerulonephritis, polyarteritis nodosa, Guillain-Barre syndrome
25
Healthcare workers have a risk of
hep B
26
Hep B is spread through
Infected blood products or sexual contact (in saliva, semen, vaginal secretions) ~ 6 weeks - 6 months
Percutaneous, sexual, parenteral, perinatal
27
Similar to acute hepatitis A
Serum aminotransferases higher on average
Utilize serologic patterns: + HBsAg, Anti-HBc, HBeAg (chronic)
hep B infection
28
how can you prevent hep B?
Handle disposable needles carefully and NOT recap
Screening of donated blood
ALL pregnant women undergo testing for HBsAG
Immunoprophylaxis reduces risk of perinatal transmission, mother may get antiviral treatment in 3rd trimester
HBIG is protective + HBV vaccine
29
How do you treat hep B?
Bed rest
N/V → IV glucose
Avoid strenuous exertion, alcohol, hepatotoxic agents
Hospitalize if:
Encephalopathy or severe coagulopathy = acute liver failure
Liver transplant
29
elevated aminotransferase levels for 3-6 months + and in majority of infected infants and immunocompromised adults
chronic hepatitis
30
Incubation 6-7 weeks with clinical illness – prodrome of anorexia, N/V, malaise, aversion to smoking, fever, enlarged and tender liver, jaundice
Asymptomatic, waxing and waning of symptoms
acute hepatitis C
31
What are RF for hepatitis C
IV drug use
Body piercing, tattoos, hemodialysis
Lower risk = sex and maternal-neonatal transmission
HIV
31
Transmission through injection of drugs
MCC of chronic liver disease, cirrhosis, and liver transplantation
hepatitis C
32
33
Liver biopsy = hepatocellular necrosis and mononuclear infiltrate
LABS: Markedly elevated aminotransferases
Antibodies to HCV (confirm with assay for HCV RNA)
anti-HCV = antibodies, previous infection
hepatitis C
34
all adults 18-79 and all pregnant women should be screened for
HCV
35
How do you treat HCV?
Eradicate infection and prevent disease progression (defined as absence of HCV RNA in serum 12 weeks following completion of antiviral therapy
Sofosbuvir + velpatasvir x 12 weeks
OR glecaprevir + pibrentasvir x 8 weeks
36
does chronic hepatitis develop in hep C?
yes -- VERY OFTEN
37
Does chronic hepatitis occur in hep B?
yes
38
Most are asymptomatic; fatigue, myalgia, nausea, RUQ pain, jaundice, dark urine
In chronic hepatitis B = worse short term prognosis → acute liver failure, severe chronic hepatitis rapidly progressing to cirrhosis
hepatitis D
39
what are RF for hepatitis D?
Drug injectors
High-risk sexual behavior
HIV/HCV co infections
40
Can you only have HDV without HBV
no
41
You only have an HDV with --
HBsAg
42
Dx: detection of antibody to hepatitis D antigen (anti-HDV), HDAg or HDV RNA in serum
Check for presence of HBV virus (HBsAg)
HDV
43
How do you treat HDV?
Pegylated interferon alfa 2b
44
Prodrome of anorexia, N/V, malaise, aversion to smoking
Extrahepatic manifestations: arthritis, pancreatitis, thyroiditis, myocarditis, glomerulonephritis, monoclonal gammopathy, thrombocytopenia, aplastic anemia, Guillain-Barre syndrome
hepatitis E
45
Hepatitis E is prevalent in
international traveling to endemic areas
FULMINANT in pregnant women
46
What's the MCC of acute viral hepatitis? (and how is it transmitted)?
Hepatitis E - fecal-oral transmission
47
PE: jaundice, scleral icterus, hepatomegaly, RUQ tenderness
IgM anti-HEV in serum
ALT>AST, >1000
Past immunity = IgG HEV Ab with - IgM
hep E
48
How do you treat hep E?
3 month course of oral ribavirin (severe)
49
chronic hepatitis is often
asymptomatic
50
Chronic infection for longer than 3-6 months: viruses, autoimmune hepatitis, alcohol-associated, metabolic dysfunction-associated steatohepatitis, certain meds (isoniazid and nitrofurantoin), Wilson disease, antitrypsin deficiency, celiac disease
chronic hepatitis
51
Risk for reactivation = male sex, HBV genotype C, immunosuppression, advanced age, alcohol use, smoking, coinfection
chronic hepatitis B
52
What are the 5 phases of chronic hepatitis B?
Immune tolerant (common in infants/children)
Immune active
Inactive HBsAg carrier state
Reactivated chronic hepatitis B phase
HBsAg-negative phase
52
HBeAg+ and HBV DNA present
Serum aminotransferase levels normal
Little necroinflammation in liver
chronic hep B immune tolerant
53
HBeAg+ with aminotransferase AND HBV DNA levels elevated
Necroinflammation present in liver
Low-level IgM anti HBc present
chronic hep B immune active
54
HBeAg- with immune clearance and cirrhosis not developed
chronic hep B inactive HBsAg carrier
55
HbeAg- with rise in serum HBV DNA levels, progression to cirrhosis may occur
reactivated chronic Hep B
56
rarely patients reach this phase with Anti-Hbe detectable and everything else normal
HBsAg- hep B
57
How do you treat hep B?
Nucleoside or nucleotide analogs → lower HBV DNA and normalize ALT and histologic improvement
Entecavir or tenofovir
58
85% of acute hep C becomes
chronic
59
chronic hep C is confirmed with
detection of anti-HCV by EIA
60
How do you treat hep chronic hep C
20% progress to cirrhosis
Antivirals: glecaprevir and pibrentasvir
Sofosbuvir and velpatasvir
61
Insidious onset with some presenting with acute liver failure, following viral illness or exposure to drug/toxin
Amenorrhea, frequency of depression
Arthritis, Sjogren syndrome, thyroiditis, nephritis, UC, Coombs+ anemia
commonly young, middle-aged women
autoimmune hepatitis
62
PE: spider telangiectasias, cutaneous striae, hirsutism, hepatomegaly
LABS: serum aminotransferase >1000
Total bilirubin elevated
autoimmune hepatitis
63
autoimmune hepatitis tx
Prednisone +/- azathioprine
64
factors that predict need for liver transplantation
Age 20+ or 60+
Low albumin
Cirrhosis
anti-SLA presence
Incomplete normalization of serum AST after 6 months
65
Fever, RUQ pain, tender hepatomegaly, jaundice, anorexia and nausea
May be asymptomatic
History
Abdominal pain/tenderness, splenomegaly, ascites, fever, encephalopathy
Infection is common
alcohol-associated liver disease
66
MC precursor of cirrhosis
alcohol-associated liver disease
67
Chronic alcohol intake >80/day for men and 30-40/day in women
alcohol-associated liver disease
68
AST > ALT often by a factor of 2 or more (SIPPING)
LABS: anemia (macrocytic), leukocytosis with left shift, thrombocytopenia, mild liver enzyme elevation, ALP, bilirubin increased
Gamma-globulin increased
Folic acid deficiency
Imaging: CT w/ IV contrast or MRI
Liver biopsy: Mallory bodies, fibrosis, infiltration
alcohol-associated liver disease
69
How do you treat alcohol-associated liver disease?
Abstinence from alcohol (acamprosate, naltrexone, baclofen, topiramate, gabapentin)
Nutritional support, supplement nutritional deficiencies
Steroids
Admit when:
-Hepatic encephalopathy is present
-INR >1.6
-Total bilirubin 10+
-Inability to maintain hydration
70
stool and urine color normal, mild jaundice, no bilirubin in urine, splenomegaly with hemolytic disorders
unconjugated hyperbilirubinemia
71
hereditary or intrahepatic (asymptomatic)
Hepatocellular disease = malaise, anorexia, low-grade fever, RUQ pain, pruritus, dark urine, jaundice, amenorrhea, hepatomegaly/tenderness, spider telangiectasias, palmar erythema, ascites, gynecomastia, sparse body hair, fetor hepaticus, asterixis
Biliary obstruction = RUQ pain, weight loss, jaundice, pruritus, dark urine, light “clay” stools, stones, occult blood
conjugated hyperbilirubinemia
72
malaise, anorexia, low-grade fever, RUQ pain, pruritus, dark urine, jaundice, amenorrhea, hepatomegaly/tenderness, spider telangiectasias, palmar erythema, ascites, gynecomastia, sparse body hair, fetor hepaticus, asterixis
hepatocellular disease --> hyperbilirubinemia
73
RUQ pain, weight loss, jaundice, pruritus, dark urine, light “clay” stools, stones, occult blood
biliary obstruction --> hyperbilirubinemia
74
What can predispose someone to hyperbilirubinemia?
Dubin-Johnson Syndrome (conjugated)
Gene mutation of MRP2 (Dubin, Direct, Dark liver) with mild icterus, flares with pregnancy, OCPs, illness
75
Formation, transport, metabolism, or excretion abnormalities of bilirubin – overproduction of bilirubin, impaired hepatic uptake due to drugs, impaired conjugation (hemolysis?)
unconjugated hyperbilirubinemia
76
impaired excretion of bilirubin, hepatocellular injury, biliary obstruction (viral?)
conjugated hyperbilirubinemia
77
Normal = <1
→yellowish discoloration of sclera and mucous indicates >2.5
Palpable gallbladder (Courvoisier sign) = pancreatic head tumor
Hepatocellular jaundice labs = increased bilirubin, ALP, AST, ALT, low albumin, unresponsive to Vitamin K
Obstruction = increased bilirubin, albumin, ALP, responsive to Vitamin K
hyperbilirubinemia
78
Dubin, Direct, Dark liver → asymptomatic/mild icterus, flares with pregnancy, OCPs, illness
dubin johnson syndrome
79
gene mutation of MRP2 → decreased hepatocyte excretion of conjugated (direct) bilirubin
black liver on biopsy
DJS
80
Type I: neonatal jaundice with severe progression in 2nd week that can lead to encephalopathy
Type II: asymptomatic
Crigler-Najjar syndrome
81
autosomal recessive disorder Type I (no activity), Type II Arias Syndrome (limited activity) of enzyme conversion (inability to convert indirect → direct)
Crigler-Najjar syndrome
82
Dx: elevated total bilirubin, no elevation in LFTs
→ Type I: 20-50
→ Type II: 7-10
Crigler-Najjar syndrome
83
How do you treat CN syndrome?
Type I: phototherapy, criss = plasmapheresis, liver transplant
Type II: phenobarbital if needed
84
asymptomatic to transient episodes of jaundice during stress, fasting, ETOH, illness
gilbert's syndrome
85
hereditary reduced UGT activity/production → decreased unconjugated bilirubin uptake
Gilbert's syndrome
85
Dx: elevated bilirubin, no elevation in LFTs
gilbert's syndrome
86
Do GS or DJS need treatment?
no
87
Abdominal distention, recent weight gain, vague abdominal discomfort, dyspnea
common in cirrhotic patients
ascites
88
Accumulated fluid in the peritoneal cavity
Most common decompensation from cirrhosis
ascites
89
Clear on PE – US, imaging
→ all new ascites should undergo diagnostic paracentesis (check if SBP is present)
SAAG gradient 1.1g/dL
SAAG >1.1 = cirrhosis or cardiac ascites (more protein)
SAAG <1.1 = infection, malignancy (less protein)
ascites
90
SAAG > 1.1
cirrhosis or cardiac ascites (more protein)
91
SAAG <1.1
infection, malignancy (less protein)
92
How do you treat ascites?
Na+ restriction <2g/day, diuretics
Spironolactone + lasix
Refractory = large volume paracentesis
>5L removed = add albumin replacement
93
Wide range of neuropsychiatric changes → subclinical to comatose
Grade 1: altered consciousness, sleep-wake reversal, memory impairment
Grade 2: drowsy, confusion, bizarre behavior, disorientation
Grade 3: lethargic/stuporous, another planet
Grade 4: coma
Asterixis, AMS
hepatic encephalopathy
94
GI bleeding, constipation, infection, hypovolemia, opioids/sedatives, TIPS
hepatic encephalopathy
95
AMS/cognitive impairment secondary to cirrhosis from toxic accumulation → increased ammonia → upregulation of GABA with more dysregulation
hepatic encephalopathy
96
elevated ammonia
hepatic encephalopathy
97
how do you treat hepatic encephalopathy
Decrease intestinal ammonia production/increase excretion
– lactulose - neutralizing ammonia
– rifaximin
eat!
98
Often asymptomatic, mild RUQ discomfort
Hepatomegaly
Signs of portal HTN = liver fibrosis/cirrhosis
fatty liver/ non-alcoholic fatty liver disease, (MDAS)
99
What predisposes someone to fatty liver?
Obesity
Diabetes
Hypertriglyceridemia
– psoriasis, soft drink/red meat consumption, ambient air pollutants, cholecystectomy
100
Excess hepatic fat = steatotic liver disease
M =
Overweight or obesity, Type 2 diabetes, impaired glucose regulation, HTN, dyslipidemia
Extremely common cause of mildly abnormal LFTs
Nonalcoholic fatty liver = benign accumulation of TGs, unassociated with malignant potential
Nonalcoholic steatohepatitis (NASH) = liver cell injury and death, inflammation, fibrosis
fatty liver disease
101
Elevated aminotransferase levels, elevated ALP, hepatomegaly, steatosis
Liver biopsy = macrovesicular steatosis w/ or w/o inflammation and fibrosis
FIB-4 score, NAFLD score
fatty liver disease
102
what's the treatment for fatty liver disease?
Vitamin E
Thiazolidinediones reverse insulin resistance (leads to weight gain)
Metformin
Pentoxifylline
semaglutide/liraglutide
ACEI
Surgery if BMI > 35, liver transplant
Weight loss, dietary restriction, increased fiber, moderate exercise, Mediterranean diet, fasting
103
Paradox – intrahepatic vasoconstriction and resistance with extrahepatic vasodilation increasing blood flow
portal HTN
104
Insidious onset of upper abdominal pain, hepatomegaly, new/worsened ascites
Classic triad: ascites + hepatomegaly + RUQ abdominal pain developing rapidly
hepatic vein obstruction (Budd-Chiari syndrome)
105
What are RF for hepatic vein obstruction
Hereditary
Hypercoagulable states (disorder, pregnancy, surgery, meds), intra abdominal malignancy, surgery, inflammation, cirrhosis
106
obstruction/narrowing of hepatic veins as a portal vein DVT – NONcardiac hepatic outflow blockage → decreased liver drainage
MCC of portal HTN in children
hepatic vein obstruction (Budd-Chiari syndrome)
107
MCC of portal HTN in children
hepatic vein obstruction (Budd-Chiari syndrome)
108
Dx: Doppler US of liver, CT, MRA
PE: tender, painful hepatic enlargement
Biopsy = “nutmeg” liver
hepatic vein obstruction (Budd-Chiari syndrome)
109
How do you treat hepatic vein obstruction (Budd-Chiari syndrome)?
Manage hypercoagulable conditions, ascites
Antigulation x 3 months
-> lifelong in Budd Chiari syndrome
Angioplasty, stenting, TIPS
110
Undetected until new decompensation or deterioration - often asymptomatic
Malaise, weight loss, jaundice, abdominal pain, hepatosplenomegaly
hepatocellular carcinoma
111
Viral cause of cirrhosis (HCV, HBV) is a huge RF for
hepatocellular carcinoma
112
Cirrhosis-associated
hepatocellular carcinoma
113
CT/MRI with contrast enhancement
US for nodules
Dx: tissue biopsy of liver
hepatocellular carcinoma
114
How do you treat hepatocellular carcinoma?
Eradicate viral infection, chemo, surgical resection, local treatments, transplant
115
what's the surveillance for hepatocellular carcinoma?
with chronic HBV infection, cirrhosis with HCV, HBV, ETOH use
Alpha-fetoprotein levels elevated
Standardly monitor with US + AFP levels 6 months for high risk patients
116
GI symptoms, systemic inflammatory response, kidney dysfunction, adrenal insufficiency, subclinical MI, jaundice
acute liver failure (fulminant hepatitis)
117
Acetaminophen and idiosyncratic drug reacts are MCC
fulminant hepatitis
118
Fulminant = hepatic encephalopathy within 8 weeks after onset of liver injury (INR 1.5+)
Subfulminant = 8 weeks - 6 months
Acute on chronic = deterioration in liver function often caused by infection
Viral hepatitis, heat stroke, malignancy, Budd-Chiari, Wilson, Reye, fatty liver, autoimmune, parvovirus
liver failure
119
AST + ALT elevated >5000
Blood ammonia level elevated and correlated with development of encephalopathy and intracranial HTN
AKI
liver failure
120
how do you treat liver failure?
Achieve metabolic and hemodynamic stability
Intravascular volume preservation (but avoid large-volume infusions)
Norepinephrine vasopressor, + vasopressin if persistent
Prevent hypoglycemia
Intermittent renal replacement therapy
Preserve muscle mass = enteral administration of protein (monitor ammonia)
H2 receptor or PPI prophylaxis
Broad spectrum antibiotic prophylaxis
Acetylcysteine for acetaminophen toxicity
Liver transplantation
121
When are AST and ALTs elevated
hepatocyte injury
122
When are ALPs elevated
injury to bile ducts
123
albumin decreases in --- --- and is associated with
liver disease, chronic
124
deficient clotting can result from
liver disease (usually acutely)
125
evaluate:
HBsAg+
Anti-HBc IgM+
HBeAg+
acute hepatitis B
126
evaluate:
Anti-HBs +
vaccination
127
evaluate:
Anti-HBs+
Anti-HBc IgG+
Anti-HBe+/-
recovery/immunity
128
evaluate:
HBsAg+
Anti-HBc IgG+
HBeAg+
chronic hepatitis B
129
Prolonged appearance of HBeAg increases the likelihood of what?
chronic hepatitis B
130
HCV RNA +
anti HCV+/-
acute hep c
131
anti-HCV +/-
HCV RNA -
resolved hep c
132
HCV RNA +
anti-HCV +
chronic hep c
133
HCV RNA is more
specific
134
with HBeAg+ or HBeAG- chronic Hep b, risk of cirrhosis and HCC correlates with
serum HBV DNA level
