1. Liver Disease in Primary Care
Trish Berglund, PAC
4/8/2016
IAPA: Sun Valley Conference 1

2. DISCLOSURE
I have no known conflicts of interest

3. OBJECTIVES Describe the signs and symptoms of hepatic disease
Order the labs/test to evaluate the patient with liver disease
Initiate treatment of the patient with liver disease
Make an appropriate and timely referral to a specialist for the patient with liver disease 3

4. ANATOMY 4

5. Why Is the liver so Important?
Lungs have ventilators, kidneys have dialysis, hearts have pacemakers and LVAD’s….
The liver does much of it’s work at a cellular level, there is no replacement or bridge
Protect this vital organ!

6. Case One
CC/ID: 38 YO WF presents for a routine visit. VSS, PE nl, Labs: WBC 9.0, HCT 38, PLTS 204, AST 20, ALT 19, ALB 4, TSH 2.0, Cr Meds Levothyroxine, Naproxen, Prilosec.
A) Renew meds and schedule a 12 mo f/u visit
B) Get more labs
C) Refer

7. PHYSIOLOGY Homeostasis & Metabolism Hemostasis
Guards against infection – makes immunoglobulins, cell walls of RBC’s
Filters toxins
Most drugs are metabolized by the liver
Alcohol can alter metabolism of other drugs like acetaminophen
.va.gov Hepatitis C, Guide for patients 7

8. Homeostasis & Metabolism:
Gluconeogenesis: Primary function of the liver. This is the last to go when the liver fails. No sugar is incompatible with life.
Ketogenesis/fat metabolism
Digestion- Bile/fat metabolism
Stores vitamins, sugars, fats, nutrients
Cirrhosis: A Patient’s Guide

9. Hemostasis Coagulation – produces proteins involved with clotting
Oncotic pressure – Albumin produced
Red blood cell development. This is in part due to lipid metabolism. Lipids are the substrate for cell walls
Problems with the liver can lead to thrombocytopenia- low platelets (splenic sequestration)
Maddrey, Atlas of the Liver ,2004.

10. 1. Self assessment
Which functions best reflect the physiology of the liver?
A) Proton pump inhibition to protect gastric mucosa and suppress acid production
B) Homeostasis, Hemostasis, gluconeogenesis, filters toxins and metabolizes drugs
C) Cell wall synthesis via amino acid metabolism
D) Sequestration of platelets by the spleen

11. Case Two
CC/ID: 48yo F presents for f/u of HTN, HLD and GERD. Complains of fatigue, myalgias and irritabiility. P 76, BP 168/86, BMI 37. Meds: Losartan, Atorvastatin & Pantoprazole. Labs from last week: WBC 6, HCT 40, PLTS 187, AST 86H, ALT 88H, Alk phos 92H, ALB 4.3
A) Refill meds, recheck 12 months
B) More tests
C) Refer to gastroenterology

12. Evaluating Elevated LFTs
Is the patient sick or not sick?
If not critical, observe, repeat to confirm
Hepatocellular, cholestatic and infiltrative patterns can coexist
Use exam and history to help guide you

13. LIVER TESTS – BASIC
AST/ALT: intracellular enzymes released due to necrosis/inflammation of hepatocyte
AST also in heart, skeletal muscle, brain, kidney
ALT is more liver specific
Alkaline Phosphatase: enzyme bound in bile duct membranes, leaks w/irritation, back pressure
Total Bilirubin: yellow substance from Red cell breakdown
Albumin prevents fluids from leaking out of blood vesses into tissue, protein synthesis
Total Protein: Alb + Globulins, transport, immunity
Sabatine, Pocket Medicine, 2011 13

14. BASIC PATTERNS Hepatocellular – liver cells irritatated
Cholestatic – Cells of the bile ducts irritated
Isolated hyperbilirubinemia – Bilirubin production defect
Infiltrative – Foreign / proliferative cells
Limdi, 2003, Eval of abnormal LFT

15. Hepatocellular patterns
Hepatocellular: defined by hepatocyte injury
AST, ALT elevations +/- up bilirubin and Alk Phos due to hepatocyte dysfunction.
Look for Viral, Toxin damage, Ischemia, Autoimmune, NAFLD, Vascular & Hereditary, other labs play a role
AST>ALT 2:1 ratio, suspect alcohol usually less than 400, if chronic elevated MCV, high HDL

16. Hepatocellular patterns, cont
ALT> AST 2:1 ratio – suspect fatty liver disease Minimal rise in AST/ALT is noted in Fatty liver disease, rise and fall correlates with weight
↑↑↑ ALT and AST elevations >1000
Acute viral hepatitis, Acute autoimmune hepatitis, Acetaminophen toxicity, Ischemia “Shock Liver”
Synthetic function – Lo albumin & Hi PT/INR– Severe hepatocellular dysfunction

17. Cholestatic patterns
Cholestatic: defined by disruption of bile flow or biliary injury
Alk Phos and bilirubin up +/- up AST/ALT.
look for bile duct irritation/inflammation/obstructions.
Imaging plays an important role. US, CT, MRCP
Can be intra or extrahepatic

18. Cholestatic patterns, cont.
Elevated Alk phos and Bili, +/- AST/ALT
Alk phos is also made in the bone so if there is isolated elevation and no liver source check vitamin D level, PTH and look for causes of increased bone turnover, fracture or malignancy. Alk phos can be elevated in pregnancy
Imaging to determine duct dilation, if not dilated, hepatitis, cirrhosis , meds, sepsis, post-op or Primary biliary cirrhosis
If dilated - biliary obstruction: choledocolithiasis, cholangiocarcinoma, pancreatic CA, sclerosing cholangitis

19. ISOLATED HYPERBILIRUBINEMIA
Defective conjugation: Check a direct bilirubin, subtract total bili from direct bili to get indirect bili, if indirect >direct – Gilbert’s
Overproduction – hemolysis, faulty red cell
production, hematoma reabsorption, PE.
Defective excretion – Dubin-Johnson

20. INFILTRATIVE PATTERN Alk phos up, near normal bili, Ast, Alt
Malignancy: HCC, mets, lymphoma
Granuloma: TB, sarcoid, histoplasmosis
Abscess: Amebic, bacterial
Other – meds/idiopathic.
Sabatine, Pocket Medicine 2011

21. Pearls AST/ALT elevations in cirrhosis may be minimal
Abrupt rise in bilirubin – other than just cholestatic process consider GI bleeding or hemolytic process *either could be accompanied by elevated K+

22. Clues for Chronic Disease
Lipid panel: Total cholesterol, LDL, HDL, triglycerides. Exceptionally low LDL and pt not on statin, consider cirrhosis.
CBC - Hg/HCT, WBC. PLTS, MCV. Cirrhotics can be pancytopenic, MCV elevated with ETOH abuse/use

23. 2. Self assessment Which statement is incorrect?
A)Hepatocellular liver disease affects hepatocytes causing release of AST/ALT
B)Infiltrative liver disease could be from meds, HCC, granulomatous disease or abscess
C)Hyperbilirubinemia is from eating excess yellow/orange vegetables.
D)Cholestatic liver disease is intrahepatic irritation of bile ducts or extraheptic blockage

24. Case 3
Mr. J is a 78 YO male who’s been told by his provider that he has Hepatitis A as the cause of his yellow skin and eyes but his malaise has progressed, he has profound fatigue, depression and worsening jaundice so he’s come to the ED for further eval.
VS: P86, BP 130/80, WT 156, O2 sat 96% RA
PE: Looks concerned, down, tired, no SI, skin yellow, scleral icterus, RR, LCTA, abd soft, Liver edge 3FB below R rib,

25. Case 3, continued
Labs: WBC 9, PLTS 147L, T. bili 17H, Alk phos 287H, AST 87H, ALT90. Hep A IGG+, Hep A IGM - , Hep BsAb -.
The Resident sent his intern to the ED to admit and turns to you and says, “This guy doesn’t have acute Hep A…” What to do – it is 5PM?
A) Examine RUQ, food/travel hx, order imaging
B) Admit for fluids, serial labs, supportive
C) Call surgery

26. Patient with Jaundice
Yellowish discoloration of tissue from deposition of bilirubin
Bilirubin is derived from degrading red blood cells
Serum bilirubin at least 2.5 or higher can result in jaundice
Can be acute or decompensation of chronic liver disease
History: Duration, sick contacts, contaminated food/water, sexual practices, IVDU, medication – prescribed, herbal and OTC, ETOH, itching, color of urine/stools, abdominal pain, family history
Exam: painless/ Painful, Evidence of sepsis, IVDU, Caput medusa/ other exam findings of chronic liver disease, ascities/acute abdomen, encephallopathy. 26

27. Jaundice, cont. Acute causes
Intracellular: Decompensation of chronic liver disease, alcoholic hepatitis, acute viral hepatitis – HBV, HCV, HAV, EBV, HIV, Acute autoimmune hepatitis, Drugs – acetaminophen, HAART, Valproate, general anesthesia, isoniazid
Extracellular – Sepsis/hypotension, gallstone disease, hemolysis, malignancy – pancreatic, metastatic

28. Jaundice Cont
Labs include LFT’s (AST/ALT, Alk phos, protein, albumin, total bilirubin), CBC, INR, Acute hepatitis panel: Hep A IGM, Hep B sAG, HCV AB, EBV, CMV
Imaging includes: US, CT, MRCP
Greenberger, Norton; et alt. Current Diagnosis and Treatment: Gastroenterology, Hepatology, and Endoscopy. McGraw-Hill, 2009,

29. Case follow-up
Mr. J had painless jaundice, imaging revealed a mass at the head of the pancreas, GI performed ERCP, stent placed to drain bile, T. Bili dropped, Palliative care before discharge.

30. 3. Self assessment The history from a jaundiced patient includes:
A) ROS for wt loss, abd/joint pain, LMP
B) Drugs: Legend, scheduled and supplements
C) Use of tanning beds, spray/topical tan agent
D) Surgical hx of the biliary tract
E) Soc hx: Etoh, illicits, sexual hx.
Best Answer :1) all above 2) A,D,E 3) A,B,D,E.

31. Case Four What is our next step?
CC/ID: 27yo F has a week of malaise and fatigue, slight RUQ pain and has noted a slight yellow tinge to her skin.
VSS, PE slight jaundice and scleral icterus, Abd: Soft, non-specific abd pain to deep palp.
Labs: AST 1259, ALT 1320, PLTS 180, AlB 4, Bili 5.2
Laboratory findings — Laboratory abnormalities may include marked elevations of serum aminotransferases (usually >1000 IU/dL), serum total and direct bilirubin, and alkaline phosphatase [27]. The serum alanine aminotransferase (ALT) is commonly higher than the serum aspartate aminotransferase (AST). The serum aminotransferase elevations precede the bilirubin elevation, with the peak bilirubin concentration occurring after the peak aminotransferase elevations. Serum bilirubin levels above 10 mg/dL are common. Other laboratory abnormalities include nonspecific elevations of acute phase reactants, elevated erythrocyte sedimentation rate, and increased immunoglobulins.
What is our next step?

32. Case Four continued
Initial Labs: AST 1259, ALT 1320, PLTS 180, AlB 4, Bili 5.2
Hepatitis Panel
Acute Hep A
Hep A IgG-
Acute Hep B
Hep A IgM+
Both acute hep A and B
Hep B sAG-
D) Acute Hep A, Immune B
Hep B sAB+
Hep BcAb-

33. Hep A/B Serology Keep calm, carry on IgM – Acute response, comes first
IgG – Late response, signals immunity
Antigen forms in response to the acute attack
Antibody is the protectant response, immunity
Study your lab interpretations
Look up Hepatitis A/B serology
Supportive care, reportable disease

34. Case Four: Follow-up
She returns for a 6 week f/u with normal vital signs, neg ROS and nl PE. AST 30 ALT 24, Alk phos 80, PLTS 198. Hep A IgM-, Hep A IgG+, Hep BsAG-, HepBcab -, Hep B sab +
Symptomatic Hep A likely from a food borne source. Spontaneous recovery. Hep A vaccine Vaccinated against Hep B and Immune,

35. Case Five
CC/ID: 42 YO WM here for f/u of elevated AST and an abnormal US, “Coarse, diffuse hepatocellular process”. 1st had LFT changes concurrent w/progressive weight gain and an increase in simvastatin dose. Neg for viral hepatitis, hemachromatosis screening and autoimmune disease. No ETOH, supplements or illicits. AST (15-41)
A)refill meds, f/u in 12 mo B)Advise weight loss and repeat labs in 3 months C)Refer to GI

36. CHRONIC LIVER DISEASE NASH/Fatty liver disease Gilbert's disease
Hemochromatosis
Wilson's disease
Hepatitis B and C
Autoimmune Hepatitis
Alcoholic liver disease
Alpha one antitrypsin deficiency
Primary biliary cirrhosis
Maddrey, Atlas of the liver, 2004 36

37. Disease specific Tests
ANA : Autoimmune Hepatitis
Alphafetoprotein: Liver CA
Alpha 1 antitrypsin: Deficiency
Ceruloplasmin: Wilson's disease
Direct bilirubin
Iron panel, ferritin, hemochromatosis genetics
5’nucleotidase, G-GTP 37

38. NASH/FATTY LIVER DISEASE
Nonalcoholic fatly liver disease is a spectrum from simple steatosis to nonalcoholic steato hepatitis. Liver biopsy may be necessary to diagnose
Associated with metabolic syndrome, obesity, diabetes and HLD, can coexist with excess ETOH, APAP, HCV
Asymptomatic, mild elevation of ALT>AST 2:1.
Emerging cause of cirrhosis with potential for liver cancer
Treatment is weight loss – gradual
Tolerate AST/ALT up to 3xULN before stopping statins. 38

39. GILBERT'S DISEASE
Chronic disorder / variant of normal of bilirubin conjugation that causes asymptomatic elevation of Indirect > direct bilirubin. Total bilirubin – direct bilirubin = indirect bilirubin.
Isolated elevation of total bilirubin, otherwise normal liver function
Can cause jaundice, worse with fasting.
Verify normal AST/ALT , absence of hemolysis with a normal hemoglobin and reticulocyte count No bili in urine.
Does not shorten life expectancy 39

40. HEMOCHROMATOSIS Elevated ferritin >1000 or LFT elevations
Hereditary 1: people with disease
Diagnose with ferritin, iron and %FE saturation up
Transferrin sat (Fe/TIBC) >45%
Elevated ferritin >1000 or LFT elevations
Genetic C282Y, ATPB7:homo/heterozygous
Affects liver, heart, pancreas, joints
Bronze diabetes, hepatocellular carcinoma
Treatment: phlebotomy until, 50 sessions:
Transferrin sat (Fe/TIBC) <50% and Ferritin < 50 40

41. WILSON'S DISEASE Copper overload – erythrocytes, kidney, brain
1:30,000
Failure of biliary excretion of copper so it backs up in the liver
Kayser-Fleisher rings the eye – slit lamp
Detected before age 40
Ceruloplasmin, serum/urinary copper levels
Can cause acute liver disease or cirrhosis 41

42. HEPATITIS B DNA virus, others are RNA
Transmitted by blood/body fluids: IVDU, homo/heterosexual, transfusion(historic) dialysis, household contact, needlestick/healthcare, maternal fetal
8 weeks from infection to sx.
Can cause fulminant hepatitis
Fever, flu-like sx, abd pain, dark urine, clay stools, jaundice, fatigue, nausea, anorexia. HbsAg+ → immunity HbsAb+ (HBcAb+ - past exposure)
Only 30% jaundice – many subclinical 42

43. HEPATITIS B, cont. More common in Asia, 3rd world
Chronic asymptomatic carriers: HBsAg +, HBeAg+ can transmit virus
Viral threshold to begin antiviral treatment
Interferon, tenofovir, lamivudine -consider GI or ID referral
Vaccine to infants since early 1980's.
Immunize all cirrhotics, those with chronic liver disease, dialysis, health care workers, diabetes mellitus 43

44. AUTOIMMUNE HEPATITIS More common in women
Autoantibodies: Antinuclear antibody (ANA), Smooth muscle antibody (SMA), elevated serum Igg
Diagnosis of exclusion (drugs, hepatitis, inherited or metabolic liver disorders
May overlap with Primary biliary cirrhosis or Primary Sclerosing cholangitis
Liver biopsy
Treated with immune suppression – Prednisone 80% response 44

45. ALCOHOLIC LIVER DISEASE
Excess alcohol is > 7 drinks a week for women >3 in a day, >14 drinks a week for men >4 in one day. Size and metabolism.
1 drink is 12 oz 5% beer, 5 oz of 12% wine, 1.5oz of 40% hard alcohol (80 proof)
60% of patients with alcoholic cirrhosis have no signs or symptoms of liver disease
Alcohol use together with Hep B, Hep C, iron overload, hepatotoxic drugs and fatty liver disease accelerate progression to cirrhosis.
Alcoholic liver disease is a spectrum: Starts with fat infiltration -> alcoholic hepatitis(can bypass) -> cirrhosis. 45

46. Alpha 1 antitrypsin deficiency
Alpha 1 antitrypsin deficiency is a protein disorder genetically mediated (AIAT)
Rare, northern Europeans most affected
Causes accumulation of variant protein inclusions in the liver
Liver biopsy along with blood test would confirm the diagnosis
Lung disease/emphysema is also caused
Liver transplant is the only treatment

47. PRIMARY BILIARY CIRRHOSIS
Inflammation/destruction of the intra hepatic bile ducts
Rare - affects mainly middle aged women, the cause is unknown
Most are initially asymptomatic but develop fatigue, dry eyes, mouth and itching. Later jaundice, skin hyperpigmentation, hepatosplenomegaly , xanthelasmas
Elevated alk phos with normal bilirubin, antimitochondrial antibody is present, liver biopsy
Urosdeoxycholic acid (Ursodiol/Actigal) improves survival
Liver transplant is effective for end stage
Maddrey, Atlas of the Liver , 2004 47

48. Case Six
CC/ID: 55 YO WM comes for a follow up visit, offers no complaints. P 80, R 15, BP 145/90, O2sat 91%. Meds: HCTZ, simvastatin, omeprazole. ETOH 1-2 beers most PM’s, 6 pack w/Football games on TV, Tob 1PPD, no illicits. FHX: Dad died of liver CA. Labs: WBC 4.0, HCT 55, PLTS 108L, AST 120H, ALT 60, Ferritin 495H, + genetics for hemachromatosis.
A) ETOH B) Hemachromatosis C)Cirrhosis D)All

49. CIRRHOSIS
General term: end stage scaring of the liver. Multiple etiologies not revealed by liver biospy. Diagnosis combines labs, imaging, liver biopsy (GR/ST 4/4) and physical exam changes.
Compensated
Decompensated – GI bleeding, ascites, hepatic encephalopathy –> Portal HTN
THERE IS NO SAFE AMOUNT OF ALCOHOL IN CIRRHOTICS 49

50. CIRRHOSIS – PHYSICAL EXAM
Jaundice
Enlarged liver/spleen – usually painless
Small hard, nodular liver
Spider telangiectasia/palmar erythema
Asterixis/hyperreflexia, nystagmus
Facial muscle wasting
Acute Upper GI bleeding from esophageal varices (dilated blood vessels in lower esophagus)
Ascites/Umbilical hernia/spontaneous bacterial peritonitis
Caput medusa
Lower extremity -> total body edema (Anasarca)
Encephalopathy
Gynecomastia 2 3 4 50

51. CIRRHOSIS – LAB CHANGES
Platelets low, especially less than 100 with known chronic liver disease - Thrombocytopenia
Hg/HCT low – marrow dysfunction or GI bleeding – Anemia
Macrocytosis: elevated MCV
WBC’s low – Leukopenia
Above combined = Pancytopenia
Albumin low
AST/ALT can be normal to mildly elevated, both AST>ALT and AST<ALT
INR elevated and pt is not on warfarin (not protective against clotting cirrhosis is a hypercoaguable state)
LDL cholesterol especially low – 40’s
Low testosterone -> low bone density
Elevated ammonia
Paracentesis: new ascites, calculate SAAG score, cytology, culture 51

52. CIRRHOSIS - IMAGING
Abdominal ultrasound – Liver coarseness, fat, increased echogenicity, enlarged or shrunken liver, enlarged spleen, nodular, masses, every 6 months to screen for primary liver cancer, used to guide Paracentesis in ascites
Multiphase liver CT – f/u to abn RUQ US, nodular/undulating contour, ascites, varices, large or shrunken liver

53. CIRRHOSIS IMAGING, cont.
Fibro scan/bone scan
Chest x-ray – R sided effusion from massive ascites
– references for cirrhosis

54. Outpatient management of Cirrhosis
Cirrhosis targets
Hepatoma surveillance. RUQ abd US and an alpha fetoprotein every 6 months
Esophageal variceal surveillance – EGD initially and then as directed by endoscopy, every 2-3 years.
Immunizations: Hep A/B, flu, PNA,
MELD score
Advance directives
Low sodium diet, avoid NSAIDS/ETOH

55. CALCULATORS
MELD: Measure of end stage liver disease. Combines INR, T. bili, creatinine and Sodium for a calculated score of 6-40, guides transplant, f/u, risk assessment
Child-Pugh: Bilirubin, Albumin, INR(protime), ascites and encephalopathy – Score defines the degree of decompensation in cirrhosis. A, B, C
APRI: AST to Platelet Ratio Index
FIB 4: AST, ALT, Age, PLTS Both estimate fibrosis 55

56. EMERGENCY RETURN CRITERIA
Fever/shaking chills
New onset Jaundice
Altered mental status/cloudy thinking
Hematemesis, coffee ground emesis, melena or hematochesia
TELL All YOUR HEALTHCARE PROVIDERS YOU HAVE CIRRHOSIS

57. 4. Self Assessment.
Cirrhosis is a spectrum disease, pick the best sequence of progression
A) LFT’s nl, encephalopathy, asymptomatic, GIB, normal image, Ascites, death
B) Ascites, Encephalopathy, GIB, jaundice, ETOH cessation, asymptomatic, mild LFT up, death
C) HCC, Encephalopathy, asymptomatic, nl LFT, inr, AFP, GIB, ascites, death.
D) Asymptomatic, sl LFT up, continued ETOh, INR up, GIB, Encephalopathy, HCC, death

58. Liver myths/misconceptions
MYTH: Acetaminophen can not be used in cirrhotics or those with liver disease.
FACT: Acetaminophen can be used but less than 2g daily. It is safer than NSAIDS which should be avoided due to GI bleeding risk, sodium retention and renal impaiment.
Cirrhosis: A patient’s guide, 2007

59. Liver Myths/misconceptions,
MYTH: Statins harm the liver, stop with any change in LFT, do not give to anyone with any kind of liver disease.
FACT: Statin benefits usually outweight risk: Cardiac disease co-exists with liver disease. LFT’s no longer routinely recommended. Hold statins for acute liver failure. Reference: FDA Update 1/31/14

60. Liver myths, cont
Tandra S, Curr Use of statins in patients with liver disease.Treat Options Cardiovasc Med Aug;11(4):272-8.

61. LIVER MYTHS, cont.
MYTH: Cirrhosis is an instant death sentence. FACT: While it is best to avoid cirrhosis, the 10 year survival in compensated cirrhosis is 90% and the odds of transitioning to decompensated cirrhosis is 50%. The median survival time in patients with decompensated cirrhosis is ~2years.
(BMJ Group Best Practices updated 6/2012)

62. WHEN TO REFER Depends on practice
Patient is unstable – decompensated cirrhosis
Diagnosis is unclear
Ill defined findings/Abn labs/imaging
Liver biopsy (GI ->Interventional radiology)
EGD for esophageal variceal surveillance
ERCP for obstructive findings CBD, painless jaundice 62

63. WHEN TO REFER, cont.
Hepatocellular carcinoma – Liver Tumor Board or Oncology
Hepatorenal syndrome
Refractory ascites
Pregnancy

64. 5. Self Assessment
An appropriate referral to a general GI outpatient practice includes:
A) Basic serial labs, imaging, advanced labs and discussion of expectation.
B) Hep A IgG+ and Hep B sAB quant +, for interferon treatment
C)Hepatocellular CA dx by multiphase liver CT, elevated AFP in a cirrhotic
D) Febrile patient with tachycardia, hypotension, jaundice and acute RUQ pain

65. RESOURCES www.hepatitis.va.gov
ines/2009cirrhosis-quicknotes-index.asp
Uwhepatitisc.edu
AASLD.org 65

66. REFERENCES
Greenberger, Norton; et alt. Current Diagnosis and Treatment: Gastroenterology, Hepatology, and Endoscopy. McGraw-Hill, 2009,
Maddrey, Willis. Atlas of the Liver- 3rd Edition. Current Medicine, INC , ,
Limdi, J, K; Hyde, G, M. Evaluation of Abnormal Liver Function Tests. Postgrad Med J 2003;79:307–312
Sabatine, Marc S. Pocket Medicine; Fourth Edition: The Massachusetts General Hospital Handbook of Internal Medicine. Lippincott, Williams & Wilkins —3-28.
MKSAP 16, American College of Physicians Medical Knowledge Self Assessment Program, GI/Hepatology, Patrick Alguire, MD Editor 66

67. REFERENCES, cont.
American College of Physicians: Board Basics 3, Doug Paauw, MD, Editor Pgs
Mayo Clinic Internal Medicine Board Review, 10th edition, Robert Ficalora, MD, Editor in Chief, 2013, Liver and biliary tract, Pgs. 169 – 187 by John Poterucha, MD

68. THANKS Paul Baehr, MD Ellen Hunter, MD Alex Berglund, MD
Nicole Ulacky, MPA 68

69. Self Assessment Answers
1. B) Homeostasis, Hemostasis, gluconeogenesis, filters toxins and metabolizes drugs. This is the most inclusive answer.
2. C)Hyperbilirubinemia is from eating excess yellow/orange vegetables. Caritonemia results in a yellow/oraage tint to the skin, especially in light skinned people/babies and is caused from eating vetetables rich in Beta Carotene: Sweet pototoes, carrot, squash. Carotinemia does not cause scleral icterus.

70. Self assessment answers, cont.
3. 3) A,B,D,E. Generally, jaundice in not caused by tanning products. Tanning beds are associated with melanoma that can spread to the liver, this would be more rare.
4. D) Asymptomatic, sl LFT up, continued ETOh, INR up, GIB, Encephalopathy, HCC, death. This is the best answer but a, b and c are possible with the addition of co-factors to include NSAIDS, Hep A/B, surgery/general anesthesia, alcohol cessatio or alcohol relapse.

71. Self Assessment answers, cont.
5. Best answer is: A) Basic serial labs, imaging, advanced labs and discussion of expectations.
The patient in B needs reassurance -> these labs reflect immunity, the patient in C needs oncology/tumor board or GI referral with a doc to doc handoff, the last patient needs admission for sepsis.