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Gastrointestinal II Exam #2 > Jaundice > Flashcards

Jaundice Flashcards

1
Q

What is the normal pathway of BR metabolism?

A

Initially it is bound to albumin, transported to the liver, conjugated ti a water-soluble form (glucuronide), excreted into bile and converted to urobilinogen in the colon

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2
Q

Which enzymes are elevated in hepatocellular disease?

Which is more specific for liver injury?

A

AST/ALT

ALT is more specific than AST for liver injury

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3
Q

Which enzymes are elevated in cholestatic disease?

A

ALP and BR

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4
Q

“True” liver function tests include (4)

A

PT/INR

Albumin

Cholesterol

Ammonia

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5
Q

DDx considerations for diseases with unconjugated jaundice (3)

A

Hemolytic syndrome

Gilbert syndrome

Crigler-Najjar syndrome

***possibly viral hepatitis (can be both)

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6
Q

DDx considerations for diseases with conjugated jaundice (5)

A

Hepatitis

Cirrhosis

Obstruction

Dubin-Johnson syndrome

Rotor syndrome

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7
Q

What should be evaluated for on a CBC in a patient with jaundice?

A

Anemia and thrombocytopenia

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8
Q

What chemistry labs should be ordered for a patient presenting with jaundice? (3)

A

AST/ALT, total BR, ALP

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9
Q

Diagnosing obstructive jaundice (conjugated) typically begins with what?

A

US

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10
Q

Which antibodies suggest an acute vs. chronic viral hepatitis: IgM and IgG?

A

IgM: acute

IgG: chronic

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11
Q

Stool appearance in acute hepatitis:

A

Acholic stools

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12
Q

What are 3 staples of labs that should be done in a patient presenting with acute hepatitis?

A

CMP (AST/ALT, BR, ALP, albumin, renal function)

PT/INR

Acetaminophen level

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13
Q

What is the #1 risk factor for HAV?

A

International travel

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14
Q

“Aversion to smoking” =

A

HAV

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15
Q

Unique symptoms of HAV (3)

A

Enlarged and tender liver

Jaundice

Acholic stools

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16
Q

What liver enzymes are markedly elevated in HAV?

Elevation of which labs indicate cholestasis?

What is the best test for diagnosing acute hepatitis A?

A

AST/ALT

Elevated BR and ALP

IgM anti-HAV Abs

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17
Q

What is the duration/progression of HBV?

A

Acute illness usually subsides over 2-3 weeks -> complete clinical and laboratory recovery by 16 weeks

5-10% will become chronic

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18
Q

Marked cholestasis is not a feature in…

A

HBV

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19
Q

When are aminotransferases highest in HBV?

A

Early in the course

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20
Q

Positive serology in the window period in HBV (1)

A

IgM Abs

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21
Q

Positive serology in acute infection in HBV (4)

A

HBsAg
IgM Abs
HBeAg
HBV DNA

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22
Q

Positive serology in prior infection of HBV (2)

A

Anti-HBsAg

IgG Abs

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23
Q

Positive serology in chronic infection of HBV (5)

A 
HBsAg
IgM Abs
IgG Abs
HBeAg
HBV DNA
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24
Q

What does HBeAg indicate?

If it persists past 3 mo…

A

Viral replication and infectivity

There is an increased likelihood of chronic HBV

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25
Q

What does HDV require for its replication?

A

Requires HBV for replication

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26
Q

Co-infection of HCV has been found in at least 30% of…

A

Patients with HIV infections

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27
Q

How does cholesterol levels change in chronic HCV?

A

Decrease in serum cholesterol

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28
Q

What is the recommendation for HCV screening?

A

Screen people born between 1945-1965 (baby boomers)

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29
Q

HEV is most commonly known to infect:

What is the route of transmission? What spreads the virus?

A

Immunocompromised hosts

F-O route, spread by swine

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30
Q

What is the treatment for toxic and drug induced hepatitis?

A

Supportive treatment: withdraw suspected agent; include use of gastric lavage and oral admin of charcoal or cholestryamine

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31
Q

What is used to evaluate acetaminophen level?

A

Rumack-Matthew nomogram

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32
Q

What happens if acute liver failure is not recognized/treated?

A

Multiorgan failure and death

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33
Q

When should therapy for acetaminophen overdose begin?

A

Within 8 hrs. of ingestion, but can be effective even as late as 24-36 hrs.

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34
Q

What is fulminant hepatic failure?

When does subfulminant hepatic failure begin?

A

Hepatic encephalopathy development within 8 weeks of onset of ALD with presence of coagulopathy.

Subfulminant hepatic failure begins between 8 wks. and 6 mo.

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35
Q

Etiology of fulminant hepatitis

A

Massive hepatic necrosis with impaired consciousness occurring within 8 wks. of onset of the illness

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36
Q

Clinical manifestations of fulminant hepatitis include: (3)

A

Encephalopathy that may evolve to deep coma.

Liver changes: rapidly shrinking liver + rapidly rising BR + prolongation of PT + signs of confusion, disorientation, etc.

Cerebral edema.

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37
Q

What are labs/diagnostics used in fulminant hepatitis?

A

Rapidly increasing BR and marked prolongation of the PT even as the aminotransferases fall

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38
Q

What is the treatment for fulminant hepatitis? (4)

A

Supportive: maintain fluid balance, circulation, respiration

Restrict protein intake

Oral lactulose or neomycin

*Prophylactic abx (one factor that improves survival)

….maybe consider liver transplant

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39
Q

What are the terminal events in fulminant hepatitis?

What is the mortality rate?

A

GI bleeding, sepsis, respiratory failure, RF, CV damage, etc.

Mortality rate is high: >80% in patients with deep coma

40
Q

Chronic hepatitis must last longer than:

A

6 mo.

41
Q

Which extra-hepatic manifestation occurs in chronic hepatitis in a patient with HBV?

A

PAN

42
Q

Which extra-hepatic manifestation occurs in chronic hepatitis in a patient with HCV?

A

Mixed cryoglobinemia

43
Q

What age does AIH commonly present?

How do these patients appear?

A

F>M (80%); 30-50 y/o

Progressive jaundice, anorexia, hepatomegaly. abdominal pain. epistaxis, fever, amenorrhea.
Exam reveals a healthy-looking young woman with stigmata of cirrhosis.

44
Q

What lab changes occur in AIH?

A

Serum ALT > 1000, usually elevated BR

45
Q

Major treatment for AIH?

What complications may ensue?

A

Glucocorticoids

Cirrhosis
-> risk of HCC

46
Q

Alcoholic liver disease occurs most often in consumption of how much liquor daily?

A

80 g/day in men and 30-40 g/day in women

Daily:
-4 oz of 100-proof whiskey
-15 oz wine
-4 12-oz cans of beer
...all for 10+ years
47
Q

What ratio of LFTs should make you think alcohol-related?

A

2:1 AST to ALT

48
Q

Lab findings in alcoholic liver disease on CMP (5)

CBC

PT/INR

A 
CMP:
2x AST > ALT
Low albumin
Elevated ALP and GGT
Increased BR
CBC:
Anemia
Left shift leukocytosis
Leukopenia 
Thrombocytopenia in 10%

PT/INR:
Prolonged PT/INR

49
Q

What imaging is good for alcoholic liver disease?

A

US elastography which can show absence of fibrosis

50
Q

What can precipitate Wernicke-Korsakoff syndrome in patients with alcoholic liver disease?

A

Glucose administration (increases thiamine needs) and can cause W-K syndrome if thiamine is not also given with it.

51
Q

Aside from abstinence from alcohol, what is given to patients with alcoholic liver disease? (5)

A

Daily multivitamin, thiamine 100 mg, folic acid, Zn

Transfusions of RBC or plasma if needed

52
Q

Wernicke encephalopathy triad =

What is the treatment?

A

Confusion, ataxia, abnormal eye movements

Thiamine

53
Q

Korsakoff syndrome =

A

Permanent severe memory issues, confabulation (make-up stories, fabrication, etc.)

54
Q

What is needed to calculate Maddrey’s discriminant function? (2)
What value suggests a poor prognosis?

What is a beneficial therapy?

A

PT and serum BR
>32 is poor prognosis (short-term mortality)

Glucocorticoids

55
Q

Glasgow alcoholic hepatitis score predicts:

What does it evaluate?

A

Mortality in alcoholic hepatitis

GAH >9 who received glucocorticoids had higher survival rates than those who did no get glucocorticoids.
GAH <9 shows no benefit with glucocorticoids.

56
Q

How little alcohol should be consumed to make the diagnosis of NAFLD?

A

<20 g of alcohol in women and <30 g in men

57
Q

Most common cause of chronic liver disease =

Increased risk in which ethnicity?

A

NAFLD

Hispanics

58
Q

Classic tetrad in Hemochromatosis

What age is the onset?

A

Cirrhosis w/ hepatomegaly
Abnormal skin pigmentation
DM
Cardiac dysfunction

Rarely onsets before 50 y/o

59
Q

What are risks for advanced fibrosis in Hemochromatosis? (3)

What processes may suggest an increased mortality? (3)

A

Male sex
Excess alcohol consumption
DM

Hepatic and pancreatic insufficiency
HF
Hypogonadism (ED can develop in men)

60
Q

Lab/genetic abnormalities in Hemochromatosis (4)

A

HFE mutation
Mildly abnormal LFTs (AST, ALP)
Elevated plasma iron with >45% transferrin saturation
Elevated serum ferritin

61
Q

What imaging is helpful in Hemochromatosis?

A

MRI or CT

62
Q

Iron studies and HFE testing is recommended for which patients?

A

All first-degree family memers with Hemochromatosis

63
Q

What are some treatments/management strategies for patients with Hemochromatosis? (4)

A

Weekly phlebotomy therapy
Iron-rich food avoidance
PPI once iron store depletion is done
Deferoxamine (a chelating agent for patients with hemochromatosis and anemia)

64
Q

What age does Wilson disease occur?

When does liver disease in Wilson’s present?
When does neuropsychiatric disease present?

What imaging can be helpful?

A

<40 y/o

Liver Dz - adolescents
Neuropsychiatric disease - young adults

MRI of brain

65
Q

Biopsy shows Kayser-Fleischer rings. Diagnosis?

A

Wilson disease

66
Q

ATP7B mutation =

A

Wilson disease

67
Q

Most commonly diagnosed inherited hepatic disorder in infants and children =

A

a1-ATD

68
Q

Chronic HBV is endemic in which parts of the world?
Many infants can it via…

It is asymptomatic when…

A

Endemic in Asia and sub-Saharan Africa
90% of infants with maternal transmission

Asymptomatic healthy carrier state

69
Q

Which Abs are positive in chronic HBV?

A 
HBsAg
Anti-HBc (IgM)
Anti-HBc (IgG)
HBeAg
HBV DNA
70
Q

Chronic HCV may lead to cirrhosis progression in which patients?

A 
Men after 20 years of disease
Drink >50g of EtOH daily
Become infected post 40 y/o
Immunocompromised
Tobacco, cannabis and fatty liver promotes fibrosis
71
Q

Coffee slows the progression of what?

A

Chronic HCV

72
Q

Patients can have normal AST/ALT in which infection?

A

HCV

73
Q

Which viral hepatitis is curable?

A

HCV

74
Q

Passive congestion of the liver (nutmeg liver) can cause:

A

Ischemic hepatitis - ischemic hetopathy, hypoxic hepatitis, shock liver, acute cardiogenic liver injury

75
Q

What meds may help prior to admission in a patient with passive liver congestion against ischemic hepatitis?

What symptoms is associated with a worse prognosis?

A

Statin therapy

Jaundice

76
Q

The hepatojugular reflex evaluates…

What pathology is it associated with?

A

Right heart function

Nutmeg liver

77
Q

What lab is markedly elevated in right heart failure with liver involvement?

What is present is hepatic ischemia is onvolved?

A

Elevation in proBNP or BNP

Rapid and striking elevation of serum aminotransferase and LDH

78
Q

Findings on CBC in cirrhosis (2)

Chemistry findings in cirrhosis (2)

A

Anemia, pancytopenia

Glucose distrubances, hypoalbuminemia

79
Q

Definitive diagnosis of cirrhosis requires:

A

Bx

80
Q

Serum ascites albumin gradient (SAAG) =

A

Serum albumin - ascites album = SAAG

81
Q

Hyponatremia occurs in:

A

Ascites

82
Q

3 categories of routine studies of ascites fluid

A
  1. Cell count: WBC ct. with diff is most important test
  2. Albumin and total protein: SAAG is best test to classify ascites
  3. Culture and Gram stain
83
Q

Best imaging for diagnosing ascites

A

Abdominal US

84
Q

Hepatic encephalopathy =

What specific lab is elevated?

A

ALteration in mental status and cognitive function in the presence of liver failure

Ammonia, but the correlation between severity and ammonia is not that helpful

85
Q

4 stages of overt hepatic encephalopathy

A
  1. mild confusion
  2. drowsiness
  3. stupor
  4. coma
86
Q

2 major precipitants of hepatic encephalopathy

2 most common symptoms:

A

GI bleeding, constipation

Fever and abdominal pain

87
Q

Which bugs are NOT associated with spontaneous bacterial peritonitis?

A

Anaerobic bacteria

88
Q

What is the most important test to run on ascitic fluid in SBP? What level allows a diagnosis?

A

WBC ct. - >250 WBC/mcL

89
Q

What is the best treatment for recurrent SBP?

What is the best antibiotic?

What is a major cause of death?

A

Liver transplant

3rd-gen cephalosporin IV or a beta-lactam agent

Kidney injury, which develops in 40% of patients

90
Q

3 treatment options in HCC

A

Trasplant/resection

Radiofrequency ablation

Transcatheter arterial embolization (TACE)

91
Q

No satisfactory therapy exists in…

A

Primary sclerosing cholangitis

92
Q

Major treatment option for primary biliary cirrhosis:

A

Ursodeoxycholic acid

93
Q

What can occur as a consequence of hepatic v. obstruction (Budd-Chiari syndrome)?
What is associated with it?

What are the symptoms?

A

RSHF -> nutmeg liver
Hypercoagulibility

RUQ pain, jaundice, splenomegaly and ascites

94
Q

What is the screening test of choice for Budd-Chiari?

A

Contrast-enhanced US (CEUS)

95
Q

Window period of HBV

What test must be done if you suspect this?

A

Period between HBsAg disappearing ad HBsAb appearing. May last a few weeks, but the patient is still considered to have acute HBV.

Both tests may be negative, but disease is still there. Must check IgM!

96
Q

Positive serology in immunization of HBV (1)

A

Anti-HBs (HBsAb)

97
Q

When you see “pyogenic gangrenosum” you should think of…

A

Ulcerative colitis

Gastrointestinal II Exam #2 (3 decks)

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