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Gastroenterology > Chronic Hepatitis and Hepatocellular Cancer > Flashcards

Chronic Hepatitis and Hepatocellular Cancer Flashcards

1
Q

chronic hepatitis

A

-Chronic necrosis and inflammation of the liver for more than 3-6 months duration
-Abnormal LFTs
-Histologic findings
-Categorization:
-Etiology**- MC
-Grade of portal, periportal or lobular inflammation- Mild, moderate or severe
-Stage of fibrosis- None, mild, moderate, severe, cirrhosis

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2
Q

causes of chronic hepatitis

A

-Viral: HBV, HCV, HDV
-Autoimmune hepatitis
-Medications (INH, nitrofurantoin, others)
-Wilson’s disease
-Alpha 1 antitrypsin disease- associated with emphysema
-Hemochromatosis- iron metabolism
-Primary Biliary Cirrhosis/Cholangitis

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3
Q

chronic hepatitis B

A

-Chronic HBV- 8 genotypes and 4 subtypes
-257 mill people worldwide and estimated 2.2 mill in US
-Risk of progression to cirrhosis-
-Risk of hepatocellular cancer in those with cirrhosis
-Prognosis depends on histology/replication- HBeAg +

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4
Q

initial evaluation for HBV

A

-family history- important for vertical transmission
-test for HBV replication
-hepatocellular carcinoma screenings- US
-rule out coinfections - HDV
-fibrosis screenings- vibration controlled transient elastography (density), liver bx, serum fibrosis panel

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5
Q

chronic hepatitis B variations in presentation

A

-Asymptomatic (unless have decompensated cirrhosis or have extrahepatic manifestations)
-Nonspecific symptoms ie. fatigue
-Exacerbations of infection which may be asymptomatic, mimic acute hepatitis, or manifest as hepatic failure
-wide variation in presentation- asymptomatic to failure
-Physical examination:
-Normal
-Stigmata of chronic liver disease- caput medusa, varices
-Decompensated cirrhosis-jaundice, splenomegaly, ascites, peripheral edema, and encephalopathy
-liver flap- hands flap

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6
Q

extrahepatic complications of chronic HBV

A

-Due to circulating hepatitis B antigen–antibody immune complexes**
-Two major extrahepatic complications of chronic HBV are:
-1. Polyarteritis nodosa- inflammation of medium sized vessels -> Fever, fatigue, night sweats, loss of appetite, weight loss, and generalized weakness, myalgias and arthralgias
-2. Glomerular disease- membranous nephropathy and less often, membranoproliferative glomerulonephritis- Proteinuria, edema

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7
Q

identifying chronic hep B

A

-Persistence of HBeAg (for a variable period), HBsAg, and HBV DNA in the circulation; anti-HBs is not seen
-Persistence of HBsAg > 6 months after acute infection is indicative of chronic infection
-after 6 months - chronic

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8
Q

treatment of chronic HBV (dont need to know drugs names)

A

-**Who to treat based on circulating virus, HBeAg, LFTs, if have cirrhosis
-Nucleoside or nucleotide analog (entecavir; tenofovir alafenamide; tenofovir disoproxil fumarate) OR Pegylated interferon
-Nontreated patients: follow up varies based on HBeAg, HBV DNA, ALT level
-If have cirrhosis, monitor for HCC and sequela of cirrhosis- US, AFP q 6 mos , EGD
-AFP- liver tumor marker

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9
Q

chronic hepatitis D

A

-Co-infection can increase the severity of acute hepatitis B
-Does not increase risk of chronic hepatitis B
-Superinfection in pt with chronic hep B -Long-term HDV infection is the rule also Worsening of the liver disease
-Treatment: Interferon alpha 2a-relapse common (dont need to know)

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10
Q

chronic hepatitis C

A

-2.4 million in US
-Majority remain asymptomatic and well compensated with no clinical sequelae of chronic liver disease!
-1/3 serum aminotransferases normal
-5 to 30 percent develop cirrhosis over a 20- to 30-year period of time
-Increased risk of hepatocellular ca

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11
Q

increased likelihood of progression of liver disease in chronic HCV

A

-Older age
-Longer duration of infection (most important)
-Advanced histologic stage and grade
-Genotype 1
-Concomitant other liver disorders (alcoholic liver disease, chronic hepatitis B, hemochromatosis, alpha 1-antitrypsin deficiency, steatohepatitis)
-HIV infection
-Obesity (fat in liver aggravates), DM
-Etoh intake >50g

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12
Q

clinical findings and extrahepatic complications with HCV

A

-Similar as chronic hepatitis B
-Fatigue and sleep disturbances mc symptoms
-Jaundice rare
-Extrahepatic complications:
-Hematologic diseases- essential mixed cryoglobulinemia and lymphoma
-Renal disease- membranoproliferative glomerulonephritis
-Autoimmune disorders- thyroiditis
-Dermatologic conditions- porphyria cutanea tarda and lichen planus
-Diabetes mellitus

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13
Q

initial evaluation of chronic hep c

A

-Evaluation of patients with Chronic Hep C is the same as Hep B
-H&P
-FH
-Routine Labs
-Tests for HCV replication and genotype
-Tests to r/o other viral coinfections
-Tests to screen for HCC
-Tests to screen for fibrosis

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14
Q

ALT

A

-not a marker for liver disease

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15
Q

treatment of chronic HCV

A

-F/u monthly
-Quantitative HCV RNA test at week 4 of therapy
-Virologic response to treatment- viral load at 12 weeks following the cessation of therapy
-HCC screening for all with h/o Chronic Hep C with advanced fibrosis:
-LFTs, U/S, AFP q 6 mos
-EGD

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16
Q

autoimmune hepatitis

A

-Chronic hepatitis of unknown etiology
-Characterized by immunologic and autoimmunologic features
-Autoantibodies and a high serum globulin concentration
-Any sex/any age- commonly in middle aged women
-Can follow viral illness
-Onset is insidious in most

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17
Q

autoimmune hepatitis presentation varies

A

-Asymptomatic patients vs debilitating symptoms
-Physical findings range:
-Normal
-Hepatomegaly, splenomegaly
-Stigmata of chronic liver disease- guy in the photo
-+/- jaundice
-Signs associated with other autoimmune disorders

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18
Q

autoimmune hepatitis diff dx

A

-Chronic viral hepatitis
-Primary biliary cirrhosis/cholangitis
-Primary sclerosing cholangitis
-Wilson disease
-Hemochromatosis
-Drug-induced liver disease
-α1-Antiprotease (antitrypsin) deficiency

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19
Q

autoimmune hepatitis: for adults with compatible clinical or lab features obtain serum…(just focus on ANA and ASMA)

A

-antinuclear antibodies (ANA)*
-anti-smooth muscle antibodies (ASMA)*
-anti-mitochondrial antibodies (AMA)
-anti-liver/kidney microsomal-1 antibodies (anti-LKM-1)
-either an immunoglobulin G (IgG) or gamma globulin level
-For patients who are negative for above, obtain:
-anti-soluble liver antigen/liver pancreas antibody (anti-SLA/LP)
-anti-actin antibodies
-typical perinuclear anti-neutrophil cytoplasmic antibodies

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20
Q

autoimmune hepatitis labs

A

-High Bili
-High AST and ALT
-Classic Type 1:
-***ANA and/or Anti Sm Muscle +
-Increased serum Gamma Globulin
-Anti-HCV can be false +

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21
Q

autoimmune hepatitis dx and tx

A

-DX: Liver bx to establish dx/severity
-Treatment: (can be self limiting) Prednisone +/- azathioprine
-Vaccinate for Hep A and B
-If cirrhosis is monitored for HCC:
-LFTs
-US, AFP q 6 mos if cirrhosis
-EGD

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22
Q

primary biliary cholangitis

A

-Rare
-Formally known as primary biliary cirrhosis
-An autoimmune disease -> environmental trigger
-90 to 95% female, and most patients 30-65 yo (often in 40s-50s)
-Usually incidental finding of elevated LFTS

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23
Q

GGT

A

-differentiate if its bone are liver pathology -> high = liver

24
Q

findings with primary biliary cholangitis

A

-Symptoms: 50-60% asymptomatic -> If any-pruritis, fatigue mc
-cholesterol deposits
-PE:-depends on stage
-Labs:
-High Alk Phos* (fractionate) >1.5 nl
-** High AMA ≥1:40
- +/- high LFTS,bili
-Imaging: MRCP-shows hepatic biliary duct disease

25
Q

primary biliary cholangitis dx and tx

A

-Dx: High AMA, high Alk Phos, Bx
-Treatment: Ursodeoxycholic acid
and Replacement of fat-soluble vitamins if deficient
-Monitor: LFTs, Bone density (associated), TFTs
-If cirrhosis:
-US, AFP q 6 mos
-EGD

26
Q

primary sclerosing cholangitis

A

-intra AND EXTRAHEPATIC BILE DUCT
-large ducts- youre able to stent these
-males>females
-associated with- inflammatory bowel disease (ulcerative colitis)

27
Q

primary biliary cholangitis vs primary sclerosing cholangitis

A

primary biliary cholangitis
-female > male
-intrahepatic bile ducts
-small ducts
-associated with sjogrens syndrome

primary sclerosing cholangitis
-intra AND EXTRAHEPATIC BILE DUCT
-large ducts- youre able to stent these
-males>females
-associated with- inflammatory bowel disease (ulcerative colitis)

28
Q

hemochromatosis

A

-Increased accumulation of iron as hemosiderin in organs especially liver
-Autosomal recessive disorder- Homozygous for C282Y2 mutation mc
-*Not all who are homozygous for HFE C282Y variant develop iron overload and clinical HH. Other genetic and/or environmental factors, medical conditions, dietary iron intake, and blood loss play a role.

29
Q

signs and symptoms of hemochromatosis

A

-Nonspecific symptoms-fatigue, lethargy, apathy
-Often asymptomatic or nonspecific symptoms until >40yo in males and after menopause in females (periods balance females out up until menopause)
-Symptoms attributable to iron overload:
-Heart failure, arrhythmias, type 2 diabetes, hypogonadism, cognitive changes, arthropathy, bronze-colored skin
-Untreated, can develop cirrhosis, hepatocellular cancer (HCC)

30
Q

hemochromatosis labs

A

-Mildly elevated LFTs
-High Ferritin/iron/transferrin saturation
-HFE gene mutation
-high iron -> HFE gene mutation+ -> phlebotomy

31
Q

alcoholic liver disease

A

-Excessive alcohol can cause steatosis (fat deposition in liver), steatohepatitis (irritation due to fat in liver) and cirrhosis
-One of the most common causes of cirrhosis in the US
-Often reversible
-Acute or chronic inflammation and parenchymal necrosis
-Typically drink 100g/day for > 20 years - Risk increases if obese or liver ds
-Rule out other causes of liver disease-acute and chronic -viral, medication-induced, biliary obstruction, Wilson’s ds, autoimmune hepatitis, alpha 1 antitrypsin, NAFLD, etc

32
Q

alcoholic liver disease signs and symptoms

A

-Varies:
-asymptomatic hepatomegaly (common) to rapidly fatal acute illness or end stage cirrhosis
- +/- :
-Anorexia
-Nausea
-Hepatomegaly
-Jaundice
-Severe ds: Abdominal pain/tenderness, splenomegaly, ascites, fever, encephalopathy

33
Q

alcoholic liver disease labs

A

-AST>ALT** usually by 2x rarely >300 -> only time this happens (SLOSHED)
-High alk phos, GGT, bilirubin
-Can have:
-Anemia - damaged bone marrow, poor diet (B12, folate), varices
-Thrombocytpenia in 10%
-Prolonged PT
-Decreased albumin

34
Q

alcoholic liver disease imaging and dx

A

-Imaging:
-US/CT/MRI: -Detects steatosis, cirrhosis, ascites and Can r/o biliary obstruction, mass
-Transient elastography

Liver Biopsy-often not necessary:
-Steatosis: micro- or macrovesicular steatosis
-Hepatocellular ballooning with cytoplasmic rarefaction
-Infiltration by neutrophils or lymphocytes
-Mallory-Denk bodies
-Fibrosis
-Cholestasis
-Bile duct proliferation

35
Q

alcoholic liver disease tx

A

-ABSTINENCE!!…Fatty liver quickly resolves with abstinence
-Nutritional support
-Adequate calories and protein
-Vitamins/herbs (careful) -> limit
-Vaccinate
-Meds: Severe ds:
-Methyprednisone
-Pentoxifylline
-Screen for comp if have cirrhosis-HCC, varices
-Liver transplantation-controversial

36
Q

nonalcoholic fatty liver disease (NAFLD)

A

-Hepatic steatosis, with or without inflammation and fibrosis.
-Subdivision: nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH).
-Most common liver disorder in western world
-Risk factors:
-Obesity >40%**
-Diabetes >20%
-High TG >20%
-Meds: Steroids, amioderone, diltiazem, tamoxifen, antiretroviral therapy, endocrinopathies, starvation and refeeding, TPN

37
Q

nonalcoholic fatty liver disease signs and symptoms / labs

A

-Most asymptomatic or mild RUQ pain
-Labs:
-NL in up to 80% in NAFL (steatosis)
-Mildly elevated aminotransferases (NASH) and alk phos
-ALT>AST
-R/o other causes:
-Anti-hepatitis C
-Hepatitis B surface antigen, surface antibody, and core antibody
-Plasma iron, ferritin, and total iron binding capacity
-Serum gammaglobulin level (IgG), AMA, ASMA, ANA, ceruloplasmin, alpha 1 antitrypsin

38
Q

nonalcoholic fatty liver disease dx

A

-Diagnosis of NAFL requires all of the following:
-Hepatic steatosis by imaging or biopsy- US, CT, MRI
-Exclusion of significant alcohol consumption
-Exclusion of other causes of hepatic steatosis
-Absence of coexisting chronic liver disease
-Normal LFTS***

-Monitoring for fibrosis and Inflammation
-Elastography (vibration-controlled transient elastography, ultrasound shear wave or magnetic resonance elastography)
OR
-Serum fibrosis markers
-LFTS

39
Q

nonalcoholic fatty liver disease tx and referral

A

-Weight loss-5-7% body wt
-Diabetes tx
-Hyperlipidemia tx
-Vaccinate
-Vitamin E if NASH
-Referral:
-LFTS remain elevated despite loss of ≥5 percent of body weight
-Clinical features of advanced liver disease (eg, ascites, splenomegaly, jaundice)
-Advanced Inflammation/fibrosis on liver biopsy
-Advanced fibrosis on a noninvasive liver assessment
-MELD> 10-refer for transplant

40
Q

cirrhosis

A

-14th leading cause of death worldwide
-End result of hepatocellular injury from chronic inflammation or cholestasis
-Fibrosis and nodular regeneration
-Most Common Causes in US (80%): Chronic Hep C, alcohol, NASH (can be anything tho)

41
Q

classification of cirrhosis

A

-histologic is MC
-Micronodular
-Macronodular
-Mixed forms
-Descriptive terms rather than separate diseases
-Each form may be seen in the same patient at different stages of the disease

42
Q

determining etiology of cirrhosis

A

-Influences treatment decisions, counseling of family, predicts prognosis.
-Initial evaluation: history, physical and obtaining routine blood tests
-Findings from the initial evaluation are used to guide additional testing-bloodwork, imaging, bx
-Referred to liver specialist

43
Q

common causes of cirrhosis

A

-Alcohol and Viral hepatitis (Hepatitis B, C, D)
-Steatohepatitis
-Metabolic and/or genetic: Hemochromatosis, Wilson’s disease, a1-antitrypsin deficiency
-Cholestatic and/or autoimmune- Primary sclerosing cholangitis, Primary biliary cirrhosis/cholangitis
-Drug-induced

44
Q

clinical features of cirrhosis result from

A

-Hepatic cell dysfunction
-Portal hypertension
-Portosystemic shunting

45
Q

routine lab findings in cirrhosis

A

-Absent or minimal in early or compensated cirrhosis
-Elevated LFTs, Bili
-Low albumin
-Prolonged prothrombin time
-Anemia
-Low vs high WBC
-Thrombocytopenia

46
Q

cirrhosis dx and complications

A

-Suggestive on US
-Liver Bx (gold std but not always necessary)
-Elastography vs fibrosure
-Complications:
-UGI bleeding -Varices, portal hypertensive gastropathy, or gastroduodenal ulcer
Ascites
-Spontaneous bacterial peritonitis
-Hepatorenal syndrome
-Hepatic encephalopathy
-Carcinoma of the liver

47
Q

cirrhosis tx

A

-Treat the underlying disorder and complications
-Healthy diet, no alcohol
-Vaccinate
-Regular surveillance and early detection of hepatocellular failure- Check US and AFP q 6 mos, EGD
-Periodic MR Elastography
-End stage liver ds MELD >10: transplant evaluation

48
Q

cirrhosis: prevent decompensation

A

-Control of ascites:
-Low Na, restrict fluid, diuretics, TIPS
-Avoid ace inhibitor, NSAIDS

-Avoidance drugs poorly metabolized by the liver
-Avoid ASA and NSADIS (bleeding)
-Prompt treatment of infection (SBP)- E. coli and pneumococci most common -> IV cefotaxime
-Prompt variceal hemorrhage treatment- prophylaxes prior

49
Q

hepatic encephalopathy

A

-Disordered CNS function
-Stages:
-Mild confusion
-Drowsiness
-Stupor
-Coma

-Amonia is most measurable toxin but not solely responsible
-Diagnosis is based on characteristic symptoms and signs including asterixis
-Tx: Daily protein intake is 1.2 to 1.5 g/kg IBW
-Lactulose (causes diarrhea, poop it out), neomycin

50
Q

hepatocellular carcinoma

A

-Arise from parenchymal cells
-85% associated with cirrhosis
-Chronic hepatitis B and C infections, ETOH, NASH** hemochromatosis
-Men > women

51
Q

hepatocellular carcinoma S&S, labs, dx, staging

A

-S&S- Clinical recognition may be difficult -> Deterioration of the known cirrhotic
-Labs:
+/-High LFTS, INR, labs suggestive of cirrhosis etiology
High AFP (alpha-fetoprotein) sensitivity 66%,specificity 80%
-Diagnosis:
-Mass/nodules on US
-CT and MRI with contrast used
-Liver bx

-Staging: PET Scan

52
Q

staging of hepatocellular carcinoma

A

-TNM
-PLUS
-Child-Pugh score:
-5 factors, first 3 are blood tests:
-Bilirubin
-Albumin
-Prothrombin time
-Ascites
-Encephalopathy
-Determines severity of liver disease

53
Q

hepatocellular carcinoma tx

A

-depend on the following:
-Size, number, and location of tumors
-Presence or absence of cirrhosis
-Operative risk based on extent of cirrhosis and comorbid ds
-Overall performance status
-Portal vein patency
-Presence or absence of metastatic disease

-United States 5-year survival rate is 20% (33% if localized)

-Screening and Prevention:
-AFP and US every 6 mos if have chronic liver disease/cirrhosis
-Risk is 3-5% year with cirrhosis

54
Q

anti HBc positive and anti HBs positive

A

-prior infection
-not just vaccinated bc the core is positive
-anti-HBc neg and anti HBs positive- vaccine

55
Q

HBsAg positive, anti-HBc positive, IgM anti-HBc positive

A

-IgM- means acute

56
Q

HBsAg positive, anti-HBc positive, IgM anti-HBc neg, anti-HBs negative

A

-surface antigen positive- active
-IgM neg- chronic

Gastroenterology (20 decks)

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