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25. GI 2 Exam 2 > 1. DSA Jaundice > Flashcards

1. DSA Jaundice Flashcards

1
Q

Jaundice is caused by hyperbilirubinemia, termed icterus, most present in the sclera. It occurs as a result of overproduction, impaired uptake,conjugation or excretion, or due to regurgitation of unconj/conjugated bilirubin from damaged?

A

hepatocytes or bile ducts

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2
Q

Jaundice is seen at a bilirubin of >3mg/dl, higher mean levels of bilirubin are seen in white and hispanic men, what alone elevates bilirubin to >7mg/dL?

A

Hemolysis

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3
Q

Bilirubin is the major breakdown product of hemoglobin released from erythrocytes, initally bound to albumin, transported to liver, conjugated to water soluble form via glucuronosyltransferase to glucuronide, excreted into bile and converted to what in the colon?

A

Urobilinogen

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4
Q

Urobilinogen is excreted in the stool, a small portion is reabsorbed and excreted by the kidney, bilirubin can be filtered from the kidney only in what form?

A

Direct or conjugated form

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5
Q

Prehepatic causes of jaundice include transfusions, sickle cell anemia, thalassemia, AI disease, posthepatic causes of jaundice are gallstones, inflammation, scar tissue, or tumors blocking the flow, and what causes intrahepatic jaundice? 5

A 
Hepatitis
Cancer
Cirrhosis
Congeital Disorders (Gilbert)
Drugs
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6
Q

What type of cell injury occurs to the hepatocytes, where you see a primary elevation in AST/ALT, with ALT being more specific for liver injury than AST?

A

Hepatocyte INjury

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7
Q

What type of cell injury occurs in the bile ducts, where there is a primary elevation of alkaline phosphatase and bilirubin, also commonly causing pruritis?

A

Cholestatic Injury

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8
Q

Liver function tests, (LFTs), are common referred to as AST/ALT, ALP, bilirubin, and LDH/GGT. What are the TRUE liver function tests?4

A

PT/INR
Albumin
Cholesterol
Ammonia

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9
Q

The most common causes of unconjugated (indirect) bilirubin = jaundice are Hemolytic syndrome, gilbert syndrome, Crigler Najjar syndrome and?

A

Viral hepatitis (both)

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10
Q

The MCC of conjugated or direct bilirubinemia leading to jaundice is acute/chronic hepatitis, cirrhosis, obstruction, dubin-johnson syndrome and?

A

Rotor Syndrome

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11
Q

First steps in a pt with jaundice is to determine if hyperbilirubinemia is conjugated or unconjugated, asking is there is pruritis, duration, medications, travel history… a CBC looking for anemia and thrombocytopenia is done (prehepatic source unconjugated), what other blood work is taken?

A

CMP with AST/ALT, total bilirubin, alkaline phosphatase with FRACTIONED bilirubin (tells u indirect vs direct)

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12
Q

If alkaline phosphatase is elevated- can fractionate by ordering a GGT = gamma glutamyl transferase, if the GGT is elevated then you can expect a liver sournce, if it is normal then consider what source?2

A

bone, placenta

*ALP elevated in pediatric pt = growing bones

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13
Q

With hemolysis, you should order a CBC looking for anemia and thrombocytopenia, checking reticulocyte (high), LDH (high from cell destruction) and what which should be low?

A

Haptoglobin

peripheral smear=schistocytes /sickle cells?

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14
Q

In a patient with sickle cell anemia, one can see sickle cells, nucleated red cells consistent with asplenia, RBC with howell holly bodies and what type of cells?

A

Target cells

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15
Q

What is a benign cause of unconjugated hyperbilirubinemia due to a reduce acitivty of uridine diphosphate glucuronyl transferase (UGT1A1- AR), it causes benign, asymptomatic hereditary jaundice, increases 24-36 hours post fasting, assoc w reduced mortality from CV disease?

A

Gilbert Syndrome

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16
Q

What is an AR syndrome associated with absent UGT1A1 with no liver pathology and is FATAL in the neonatal period?

A

Crigler-Najjar Syndrome Type 1

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17
Q

What is an AD with a variable penetrance syndrome associated with decreased UGT1A1 activity, no liver pathology and is generally mild but can cause kernicterus?

A

Crigler Najjar Syndrome Type 2

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18
Q

hepatitis is inflammation of the liver, recall that chronic hepatitis is greater than 3-6months, serum fibrosure and or US elastography can ID fibrous absence or presence of cirrhosis in chronic hepatitis, when IgM / IgG are present it could indicated acute or chronic hepatitis?

A

Acute hepatitis : IgM

Chronic Hepatitis: IgG

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19
Q

Acute hepatitis is caused virally, by drugs, ischemia, bud-chiari and more, pt presents with fever malaise, myalgia, arthralgia, anorexia, nausea, vomitting, diarrhea, with an aversion to?

A

Smoking!

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20
Q

Acute hepatitis pts stools may be acholic, and it is important to review the medication list, on physical exam can see jaundice, hepatomegaly, RUQ pain/tenderness… For dx, one should check viral serology, CBC, CMP, PT/INR, and acetominophen levels (rumack matthew nomogram), complications include what two commonalities?

A

Cirrhosis of the liver which leads to hepatocellular carcinoma (HCC)

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21
Q

What hepatitis is ssRNA with a prodrome of anorexia, nausea, vomiting, mild RUQ pain, with aversion to smoking, more severe in adults than children, duration is acute and self limited with complete recovery?

A

Hepatitis A HAV

incubation 2-3 weeks, up to 6

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22
Q

Hepatitis A HAV risk factors is international travel, and fecal-oral contamination, sx include enlarged and tender liver, jaundice, children are symptomatic, also there are acholic stools, characteristic labs include an elevation of both bilirubin, alkaline phosphatase, and what other 2?

A

MARKEDLY elevated AST/ALT (both liver/bile duct elevated)

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23
Q

in Hepatitis A HAV, both IgG and IgM anti HAV are detectable so after onset, antibody to HAV (anti-HAV) is present early in the course.. the detection of IgG anti-HAV without IgM indicates previous exposure to HAV/non infectivity/immunity, what does IgM anti-body suggest?

A

current acute hepatitis A (excellent for diagnosis)

**HAV vaccine – ACUTE ONLY

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24
Q

What hepatitis is dsDNA with a prodrome of anorexia, nausea, vomiting, malaise, aversion to smoking, fever, tender hepatomegaly and jaundice, has a 2-26wk incubation (mean 8wks), acute illness subsides in 2-3 weeks and 10-15% progress to chronic?

A

Hepatitis B (HBV)

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25
Q

Hepatitis B (HBV) is common in men who have sex w men, injection of drugs, incarceration, STDs, not common from blood transfusion, symptoms include a low grade fever, with an enlarged tender liver and jaundice- variable, some may be asymptomatic and then die from GN, serum sickness or?

A

Polyarteritis Nodosa

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26
Q

Hepatitis B (HBV) is transmitted parenteral, sexually, and perinatally, perinatal transmission is endemic in sub saharan africa and southeast asia, mothers positive with HbsAg may transmit HBV via delivery, causing the risk of chronic infection in the infant as high as?

A

90%** higher likely of chronic hepatitis B in infants

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27
Q

Hepatitis B (HBV) has normal WBC, with MARKEDLY elevated aminotransferases early in the course (higher on average than HAV), but marked what is not a feature?

A

cholestasis (alk phos and bilirubin) are not elevated

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28
Q

There is a universal vaccination for Hepatitis B (HBV), 90% are acute attacks while 10% become chronic, complications, which are more common in men than women, include risk for cirrhosis (especially if coinfection w HDV) and what?

A

Hepatocellular Carcinoma

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29
Q

The Window period is between HbsAg disappearing and HBsAb appearing, which may be several weeks, but the patient is still considered to have ACUTE HBV, and the infection is only detectable with what***?

A

HbcAb IgM

IgM = Acute, IgG=chronic/long term

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30
Q

In acute infection of Hepatitis B (HBV), HBsAg is seen along with antiHBc IgM (HBcAb), HBeAg (viral proliferation and infectivity) and?

A

HBV DNA

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31
Q

In prior infection with Hepatitis B (HBV), one can see anti-HBs (HBsAb) and what other one?

A

Anti HBc (HBcAB) IgG

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32
Q

In chronic infection with Hepatitis B (HBV), there is positive HBsAg, positive anti-HBc IgM (HBcAg), and HBcAb IgG, there may also be positive HBeAg and HBV DNA which would signify?

A

that there is an acute attack of hepatitis currently

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33
Q

What is the only Ab that will be seen on serology if you are immunized to Hepatitis B (HBV)?

A

Anti-HBs or HBsAB ONLY

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34
Q

What hepatitis requires HBV for replication, is acute or chronic, endemic in the mediterranean basin spreading non-percutaneously, and in non-endemic areas (US) spreads percutaneously in HbsAg+ IV drug users/transfusions?

A

Hepatitis D (HDV)

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35
Q

Hepatitis D (HDV) can be seen on serum via anti-HDV in serum or HDV RNA, vaccinate agains HBV to vaccinate against HDV, it enhances the severity of?

A

HBV infections (acceleration of chronic hepatitis to cirrhosis)

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36
Q

What hepatitis is a ssRNA with 7 genotypes, most commonly is CHRONIC, risk factors include HIV, 90% of transfusion associated hepatitis cases, IV drug use accounts for 50% of the hepatitis cases?

A

Hepatitis C (HCV)

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37
Q

Hepatitis C (HCV) can be caused by body peircings, tattoos, intranasal drug use like cocaine, unsafe medical practices in developing world, also via bloody fisticuffs (boxing!), labs will show positive anti-HCV, with the most sensitive indicator of infection being?

A

HCV RNA**

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38
Q

Hepatitis C (HCV) will sometimes have antiHCV in serum but no HCV RNA, which means they are recovering from prior HCV infection, there are no vaccinations for HCV, there is a 50% chance of chronicity with what 2 main complications?

A

cirrhosis and hepatocellular carcinoma (HIV coinfection)

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39
Q

Hepatitis C (HCV) is a pathogenic factor in mixed cryoglobulinemia and membranoproliferative glomerulonephritis among other things, it is associated with 30% inc risk of non-hodgkin lymphoma, and a decrease in?

A

serum cholesterol and LDL lipoproteins

SAFE sex- it is curable!

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40
Q

The current recommendation for HCV is to screen people born between 1945 and 1965 (baby boomers)

A

MEOW

41
Q

What hepatitis is ssRNA and self limited, risk factors inlcude Immunocompromised hosts and is epidemic in Asia, Middle east, North africa, central america and india, transmitted fecal oral, water borne or spread by swine, PCR is positive for HEV RNA, usually acute?

A

Hepatitis E Virus (HEV)

42
Q

What type of hepatitis has on onset within 48 hours, necrosis around terminal hepatic venule, and caused by mushroom poisoning and acetominophen?

A

Dose-Dependent drug induce heptatitis

43
Q

What type of hepatitis affects a small number of poeple and may be associated with fever, rash, arthralgias, and eosinophilias, caused by isoniazid and sulfonamides commonly?

A

Idiosyncratic hepatitis

tx= supportive/withdraw agent/gastric lavage/charcoal or cholestryramine

44
Q

The number one cause of acute liver failure (ALF) is acetaminophen and the second MCC is idiosyncratic drug reaction (sporadic and not dose related) for example antiTb drugs and what, which can cause a rise in AST/ALT but rarely cause a true hepatitis?

A

Statins

45
Q

acute liver failure (ALF) can be seen with nausea, vomiting, icterus, jaundice, coagulation abnormalities and hepatic encephalopathy, and asterixis and can be diagnosed via seeing severe hepatocellular damage via a high ammonia level (>200) and in acetominophen toxicity what will the Ast/ALT be?

A

> 5000 ***

(acetominophen level determined via rumack matthew nomogram)

therapy w Nacetylcysteine should be begun within 8hours of ingestion

46
Q

Treatment for acute liver failure (ALF) includes supportive, stress gastropathy prophylaxis, N-acetylcysteine (tylenol/acetominophen OD), and early transfer to liver transplant, complications include cerebral edema and sepsis (death) and if not recognized or treated promptly leads to multiorgan?

A

failure and death

47
Q

What type of hepatic failure is characterized by the development of hepatic encephalopathy within 8 weeks of onset of ALF, with a coagulopathy present (INR>1.5)?

A

Fulminant Hepatic Failure

subfulminant occurs in 8wksto 6 months

48
Q

Fulminant hepatitis is massive hepatic necrosis and impaired consciousness in 8 weeks of onset of illnes and caused by many things, presents with encephalopathy to deep coma, rapidly shrinking liver size, rising bilirubin, prologation of PT and clinical signs of confustion, disorientation, somnolence, ascites and?

A

edema = hepatice failure with encephalopathy

*cerebral edema is common

49
Q

Fulminant hepatitis is diagnosed via rapidly* rising bilirubin levels and marked prologation of PT with AST/ALT levels falling, treatment includes support, restrict protein, oral lactulose or neomycin, liver transplant considered and *meticulous intensive care + prophylactic abx coverage which?

A

IMPROVES survival

mortality is exceedingly high

50
Q

Chronic hepatitis is characterized by chronic inflammation reaction in the liver for longer than 6 months, commonly will see fatigue, malaise, anorexia, low grade fever and jaundice, complications of cirrhosis, and in what two things may extrahepatic features predominate?

A

HBV and HCV

51
Q

Match the HBV/HCV with their extrahepatic features in chronic hepatitis?

1) urticaria, arthritis, polyarteritis nodosa, vasculitis, polyneuropathy, GN
2) mixed cryglobulinemia, porphyria cutanea tarda, MPGN, and lymphocytic sialadenitis

A

HBV=urticaria, arthritis, polyarteritis nodosa, vasculitis, polyneuropathy, GN
HCV=mixed cryglobulinemia, porphyria cutanea tarda, MPGN, and lymphocytic sialadenitis

52
Q

Chronic hepatitis is dianosed via CBC, CMP, coagulation studies and BIOPSY to histologically classify via grade (amt of necrosis/inflam) and stage (level progression based on degree of fibrosis), what is a non-invasive procedure that is done to ID presence or absence of fibrosis (cirrhosis) in chronic hepatitis?

A

Serum Fibrosure and or US elastography

53
Q

Common causes of chronic hepatitis include HBV (+/- HDV) HCV, autoimmune hepatitis, wilson’s, hemochromatosis and what, which causes lung abnlty?

A

A1-antitrypsin deficiency

54
Q

What type of hepatitis is a chronic progressive, genetic predisposition associated with other autoimmune diseases, with type 1 being the MC and classic with anti-smooth-muscle and or antinuclear antibodies ANA?

A

Autoimmune Hepatitis (AIH)

55
Q

Autoimmune Hepatitis (AIH) type 1 occurs 80% in women in 30s-50s, abrupt onset with progressive jaundice, anorexia, hepatomegaly, abdominal pain, epistaxis, fever, fatigue, amenorrhea with examination revealing a healthy appearing young woman with?

A

Stigmata of cirrhosis (spider telangectasias, cutaneous striae, acne, hirstuism, and hepatomegaly)

56
Q

Autoimmune Hepatitis (AIH) is diagnosed via CBC, CMP, INR with abnormalities including hypergammaglobulinemia, smooth muscle antibody and ANA, serum bilirubin may be increased along with what levels greater than 1000?

A

Aminotransferase levels

57
Q

Autoimmune Hepatitis (AIH) is treated with glucocorticoids and complications include cirrhosis which leads to?

A

Hepatocellular carcinoma

58
Q

Alcoholic liver disease occurs when alcohol abuse causes fatty liver, alcholic hepatitis, and cirrhosis, usually due to alch consumption greater than 80g/day in men and 30-40g/day in females, history/exam shows continuum (steatosis= fatty liver to alcoholic hepatitis (steatohepatitis) to cirrhosis), what is usually asymptomatic hepatomegaly and mild elevations in biochemical liver tests (bilirubin/ALP)?

A

Fatty liver (steatosis)

reversible on alcohol withdrawal

59
Q

What presents as asymptomatic to severe liver failure with jaundice ascites, GI bleeding and enchaplopathy, occasional cholestatic picture mimicking biliar obstruciton, 2:1 AST to ALT ratio, bilirubin and WBC elevated and on liver biopsy may see hepatocyte swelling and mallory denk bodies?

A

Alcoholic Hepatitis = 2:1 AST TO ALT *

60
Q

Alcoholic liver disease has a SAAG > 1.1, dx via CMP will show AST:ALT 2:1 ratio, serum bilirubin increased, serum ALP and GGT 3x normal limit, CBC shows anemia, leukocytosis, leukopenia, prolonged PT, folic acid deficiency, US elastography/ serum fibrosure, bx shows mallor bodies (denk) = alcoholic hyaline, which are identical to findings associated with?

A

nonalcoholic steatohepatitis (NASH)

61
Q

Alcoholic liver disease is treated with abstinence from alcohol, glucose admin increases thiamine and can lead to wenicke korsakoff if thiamine isnt given as well, daily vitamin + thiamine, zinc/folic acid, in severe alcoholic hepatitis (discriminant function >32/MELD>20) consider steroids and pentoxifylline and possibly?

A

liver transplantation (pts must substain from alch for 6 months)

62
Q

Prognosis/Complications for Alcoholic liver disease is it is the MCC of cirrhosis in the US, with inc risk of HCC, critically ill pts have 30day mortality of 50%, a maddreys discriminatn function can be calculated (>32 is bad), Model for end stage liver disease MELD score (>21 is bad), what is the difference between wernicke encephalopathy and korsakoff syndrome?

A

Wernicke: confusion, ataxia, involuntary abnl eye movements- tx w thiamine
Korsakoff: severe memory issues, confabulate/make up stories to fill in gaps- PERMANENT

63
Q

What discriminant function calculated disease severity and mortality risk in pts with alcoholic hepatitis and patients greater than 32 DF have a HIGH short term mortality and may benefit from glucocorticoids?

A

Maddrey Disciminant Function

64
Q

What score predicts morality in alcoholic hepatitis, and a score greater than 9 who received glucocorticoids had a higher survival rates than those who did not?

A

Glashow alcholic hepatitis score GAH

65
Q

What is the MCC of chronic liver disease in the US, due to obesity, DM, and hypertriglyceridemia in association with insulin resistance as part of the metabolic syndrome, increasing risk for CV disease, chronic kidney disease and colorectal cancer?

A

Non-alcoholic fatty liver disease (NAFLD)

66
Q

Non-alcoholic fatty liver disease (NAFLD) has an increased risk in hispanics, while physical acitivity and coffee consumption protect against its development, may also be caused by vinyl chloride, dx via labs showing mildly elevated AST/ALT/ALP but the levels may be normal in persons with?

A

hepatic steatosis

67
Q

Non-alcoholic fatty liver disease (NAFLD) is diadnosed via imaging, but BIOPSY is diagnostic, where there is MACROvesicular steatosis, with focal infiltration by PMN neutrophils and mallory hyaline- indistinguishable from alcoholic hepatitis and is referred to as?

A

nonalcoholic steatohepatitis NASH

68
Q

***Non-alcoholic fatty liver disease (NAFLD) = threshold of <20g of alcohol per day in women and <30g in men per day…. if more than alcoholic hepatitis

A

MEOW

69
Q

What is an autosomal recessive DO with a mutation in the HFE gene on chr6, MC in men, due to elevated iron saturation or serum ferritin, usually in pts older than 50, and will see increased accumulation of iron as HEMOSIDERIN in liver pancreas, heart, adrenals, testes, pituitary, and kidneys?

A

Hemochromatosis

**assoc with Yersinia Entercolitica**

70
Q

Hemochromatosis can cause hepatic and pancreatic insufficiency, heart failure, hypogonadism, with increased mortality, risk factors for advanced fibrosis include MALE sex, excess alcohol consumption and DM.. The classic tetrad includes cirrhosis with hepatomegaly, DM, cardiac dysfunction and?

A

Abnormal skin pigmentation ** darkening

erectile dysfunction is common

71
Q

Hemochromatosis is diagnosed via HFE gene mutation, mildly elevated AST/ALP, *elevated plasma iron with greater than 45% transferrin saturation, elevated serum ferritin, liver bx shows homozygous for C282Y, tx includes avoiding foods rich in iron, weekly phlebotomies, admin of PPI, and **?

A

chelating agent deferoaxmine (penicillamine) = pts with hemochromatosis and anemia or secondary iron overload due to thalassemia

72
Q

What disease is AR, mut to ATP7B on chr13, people under 40, resulting in impaired copper exretion into bile and a failure to incorporate copper into ceruloplasmin, accumulation seen in liver brain and eye, and causes hemolytic anemia, liver dz in kids and psych issues in young adults?

A

Wilson Disease

73
Q

Wilson disease should be considered in any child/young adult with hepatitis, splenomegaly w hypersplenism, coombs negative hemolytic anemia, portal HTN, and neurologic abnlties, including migraines, isomnia seizures, behavioral and personality changes, with a pathognominc sign of the condition being brownish or gray-green?

A

Kayser-Fleischer Ring (copper deposits in descemet membrane in cornea)

74
Q

In wilsons, you see elevated AST/ALT/ALP/Bilirubin, increased urinary copper, LOW ceruloplasmin, high hepatic copper concentration, with MRI showing cerebellar copper, and ATP7b mutation is diagnostic… treat with?

A

Chelating agent known as Penicillamine

wilson and hemochrom lead to cirrhosis

75
Q

What is a deficiency that is AR, caused by accumulation of a1antitrypsin back up inliver, MC dx ingerited hepatic disorder of infants and children, develops panacinar pulm emphysema, liver disease, **PiZZ - severe case, tx with smoking cessation/liver transplant, complication includes MICROnodular cirrhosis = HCC?

A

Alpha Antitrypsin Deficiency

76
Q

The liver during heart failure is associated with a SAAG>1.1, right HF leads to congestion and nutmeg liver, hepatojugular reflux is present and with tricuspid regurgitation the liver may be pulsatile, jaundice=worse outcome, what is SAAG?

A

High serum ascites-albumin gradient

77
Q

the liver during heart failure has a elevated BNP and the hallmark if ischemia is involved is rapid and stricking elevation of AST/ALT often greater than 5000, with an early rapid rise in the serum?

A

LDH Lactate dehydrogenase

ALP/bilirubin are mildly elevated

78
Q

What is a group of disorders characterized by chronic inflammatory reaction in the liver for 6 months, characterized by the development of liver fibrosis, to the point of formation of regenerative nodules, with decrease liver function, has 3 types: compensated, compensated w varices, and decompensated, coffee/tea consumption reduces risk?

A

Cirrhosis!

79
Q

Cirrhosis may have signs of spider talengiectasias, palmer erythema, dupuytren contractures, glossitis and cheilosis, jaundice, caput medusae, ascites, asterixis, dx via CBC will see pancytopenia and anemia with low platelet, prolonged PT (INR), CMP shows glucose distrubances and hypoalbuminemia, but a definitive diagnosis depends on?

A

BIOPSY - histologic classification via grade and stage

80
Q

Tx of cirrhosis involves abstinence from alcohol, vaccinations, NSAIDs contraindacated, ascites/edema tx with paracentesis, diuretics like furosimide and spironolactone used and what?

A

TIPS = transjugular intrahepatic protosystemic shunt

81
Q

What scoring system is used to predict the severity of cirrhosis and the risk of complications by ordering CMP/hepatic function for bilirubim/albumin/PT/INR and PE for ascites and encephalopathy?

A

Child-Pugh Scoring System

82
Q

When the SAAG (serum albumin - ascites albumin) is greater than 1.1 you know that there is a primary liver problem… if the SAAG is less than 1.1, then one can assume biliary leak, nephrotic syndrome, pancreatitis, peritoneal carcinomatosis, or?

A

tuberculosis

83
Q

What is the pathologic accumulation of fluid in the peitoneal cavity, need more than 500mL to be clinically detectable via fluid wave, shifting dulness and puddle sign, MCC by portal HTN from chronic liver disease, if SAAG is greater than 1.1 than due to portal HTN?

A

Ascites

puddle sign get on elbows and knees for 5 mins, flick tummy, + sign = sudden increase in intensity and clarity

84
Q

Ascites is MCC by portal hyper tension, tx via paracentesis and treating the cause, history may show increasing abdominal girth, associated with liver disease: alcohol comsumption, transfusions, tattoos, IV drug use, viral hepatitis, cancer= malignant ascites, fever= bacterial peritonitis, immigrants/IC hosts= Tb peritonitis, what is common oh physical exam?

A

asterixis
budd-chiari syndrome = thrombosis hepatic veins
elevated venous pressure
shifting dullness

85
Q

What is the most important test of ascitic fluid?

A

a WBC count with differential

86
Q

A PMN count of greater than 250/mcL = neutrocytic ascites is highly suggestive of spontaneous bacterial peritonitis while SAAG test is the single bes test for classification of ascites such that greater than 1.1 =?

A

due to portal hypertension/primary liver issue

Less than 1.1= non-portal HTN causes

87
Q

What causes an alteration in mental status and cognitive function in the presence of liver failure, with atypically elevated ammonia levels, asterixis (flapping tremor), dont follow ammonia levels but rather visual improvement in patient, can be caused by GI bleed or constipation, tx with lactulose, neomycin, metronidazole, rifaximin?

A

Hepatic Encephalopathy

88
Q

What carcinoma is MC in Male 4:1, tumor develops in cirrhotic liver in 5/6th decade, high incidence in asia and africa, and aflotoxin exposure contributes to it, on hx/phys you see cachexia, abd pain, fever, jaundice, asthenia, itching, tremors hepatomegaly ascites and peripheral edema?

A

Hepatocellular Carcinoma HCC

89
Q

Hepatocellular Carcinoma HCC is dx when a pt with a known liver disease develops an abnlty on US or rise in alpha fetoprotein, along with abnormal liver enzymes and function tests, tx includes surgical resection or liver transplant, radiofrequency ablation or transcatheter arterial?

A

embolization (TACE)

90
Q

Gallstones may lead to icterus/jaundice, along with acute cholecystitis, choledocolithiasis and ascending cholangitis.

A

MEOW

91
Q

What is a chronic liver disease with progressive non suppurative destructive intrahepatic cholagitis, characterized by autoimmune destruction of small intrahepatic bild ducts and cholestasis, strong female presence, age 50, asymptomatic elevation of ALP* or impaired bile excretion?

A

Primary Biliary Cirrhosis/Cholagitis (PBC)

92
Q

Primary Biliary Cirrhosis/Cholagitis (PBC) pts may have a history of urinary tract infections, smoking, hormone replacmenet therapy or hair dye, clinical presents with pruritis and progressive jaundice, xanthelasma, associated with sjogrens, raynaud, scleroderma and hypothyroidism, what serum abnormality is seen in 95% of pts?***

A

Antimitochondrial Antibodies (AMA)

93
Q

Primary Biliary Cirrhosis/Cholagitis (PBC) is associated with AMA, elevation in alk phos and GGT, bilirubin, cholesterol and IgM levels, need liver bx if AMA is negative… tx with what type of acid? (prognosis = cirrhosis but depends on age, serum bilirubin, albumin, PT and edema)

A

Ursodeoxycholic Acid

94
Q

What presents as beads on a string in 20-50y/o men, associated with IBD (UC) smoking decreases the risk along with coffee, presents as pruritus, fatigue, jaundice and osteoporosis, dx via ECRP see segmental fibrosis of bile ducts, and on liver bx (not needed) shows onion-skinning?

A

Primary Sclerosing Cholangitis (PSC) *ANCA+

No tx, liver transplant

***assoc w inc. risk of cholagiocarcinoma

95
Q

A biopsy of PSC shows degenerating bile duct entrapped in a dense, onionskin concentric scar. While a biopsy of PBC liver shows what type of lesions?

A

Florid Duct

96
Q

What causes occulsion of flow to hepatic vein or IVC, caval webs, right sided heart failure leading to nutmeg liver, due to hereditary/acquired hypercoagulable states like polycythemia vera, will see tender, painful hepatic enlargement (RUQ pain), jaundice, splenomegaly, ascites, course is frequently complicated by heptocellular carcinoma?

A

Hepatic vein obstruction (Budd-Chiari Syndrome)

*SAAG >1.1

97
Q

Hepatic vein obstruction (Budd-Chiari Syndrome) on imaging can see a prominent caudate liver lobe*, screening test of choice is contrast enhance US, imaging will show occlusion/absence of flow in hepatic veins/IVC, liver biopsy will show?

A

centrilobilar congestion = nutmeg liver

tx symptomatically, w anticoagulation, thrombolytic therapy, liver transplant

98
Q

What syndrome is due to reduce excretory function of hepatocytes, with conjugated hyperbilirubinemia, seen as benign, asymptomatic hereditary jaundice, liver is grossly darkly pigmented, bx shows centrilobular brown pigment, excellent prognosis?

A

Dubin Johnson Syndrome

*GB not seen on oral cholecystography

99
Q

What syndrome is caused by reduced hepatic uptake of bilirubin conjugates, conjugated hyperbilirubinemia, usually asymptomatic with hereditary jaundice but liver is not pigmented and the gallbladder is visualized on oral cholecystography?

A

Rotor Syndrome

25. GI 2 Exam 2 (8 decks)

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