Hepatology Flashcards

(110 cards)

1
Q

1. Understanding Liver Function Tests

4 categories of liver tests

  1. Tests for Hepatocellular damage (2)
  2. Tests for Cholestasis (2)
  3. Tests for Biliary Excretion (2)
  4. Tests for Liver synthetic function (2)
A
  1. Tests for Hepatocellular damage (AST, ALT)
  2. Tests for Cholestasis (alk phos, ggt)
  3. Tests for Biliary Excretion (tbili, dBili)
  4. Tests for Liver synthetic function (albumin, PT/INR)
  • ALT = direct damage to hepatocytes*
  • Need to order a hepatic panel to get GGT*
  • Unconjugated bilirubin = not bound*
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2
Q

Liver Function Tests

  • (1): amino alanine transferase (mainly from cytosol of _____)
  • (1): aspartate amino transferase measure cellular _____
  • (1) reflect the liver’s synthetic capacity
  • (3) measure hepatic excretory function
A
  • ALT: amino alanine transferase (mainly from cytosol of hepatocytes)
  • AST: aspartate amino transferase measure cellular integrity
  • Prothrombin time and albumin reflect the liver’s synthetic capacity
  • Bilirubin, gamma-glutamyl- transpeptidase (GGT), and alkaline phosphatase (ALP) measure hepatic excretory function

Other things in the body effect AST

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3
Q

Normal Transaminases

  • Normal ranges defined by “healthy” population (e.g. blood donors) and cutoff range ____ in different clinics/hospitals
  • True normal for alt may be elevated
  • Uln (upper limit of normal) in a young healthy patient may be higher than they should be
A
  • Normal ranges defined by “healthy” population (e.g. blood donors) and cutoff range differs in different clinics/hospitals
  • True normal for alt may be elevated
  • Uln in a young healthy patient may be higher than they should be
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4
Q

Evaluation of Cellular Integrity

  • AST may be elevated in (2)
  • An elevated GGT confirms?
  • (1) highest in toxin, drug induced, viral, or ischemic hepatitis
  • (1) more specific to liver damage
  • AST / ALT ratio
    • ALT > AST = (1)
    • AST > ALT = (1), what ratio?
A
  • AST may be elevated in myocardial infarction and musculoskeletal injury
  • An elevated GGT confirms hepatic origin
  • ALT highest in toxin, drug (ie statins) induced, viral, or ischemic hepatitis
  • ALT more specific to liver damage
  • AST / ALT ratio
    • ALT > AST – hepatitis
    • AST > ALT – alcohol - ratio >2:1
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5
Q

Examples of Typical Transaminase Elevation

Match each ratio to the cause

AST/ALT

  1. 160/80 =
  2. 120/180 =
  3. 46/78 =
  4. 400/800 =
  5. 19000/16000 =
  6. 2000/2000 =
A

AST/ALT

  1. 160/80 = Alcoholic hepatitis
  2. 120/180 = Autoimmune hepatitis (alt a bit higher)
  3. 46/78 = Chronic hep C (low grade inflammation)
  4. 400/800 = Acute viral hep C
  5. 19000/16000 = ETOH + Tylenol toxicity (severe injury)
  6. 2000/2000 = Acute hep A (equal values)
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6
Q

Alkaline Phosphatase (ALP) ↑+ GGT ↑

=

Causes (3)

A

Think Liver specifically biliary source

Obstruction

Infiltration

Congestion

(is the bile blocked/slow flowing?)

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7
Q

ALP↑ and GGT normal

(probably not (1))

  • Isoenzymes (alternative form of same ALP enzyme): ____ CA, b____
  • B____ disease?
  • I______ (malignancy
    • Endocrine: primary or secondary (1)
A

Probably not biliary disease

  • Isoenzymes (alternative form of same ALP enzyme): liver CA, biliary
  • skeletal/bone (Pagets?)
  • Intestinal (malignancy
    • Endocrine: primary or secondary hyperparathyroidism

Both ALP and GGT levels become elevated when you have issues with your bile ducts or have certain liver diseases, but only ALP will be elevated if you have bone disease.

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8
Q

Evaluation of Excretory Function

  1. (1) has origin in _____ tissues
    • May be normally elevated in late pr____, childhood/adolescence
    • Elevation correlates with ch_____ injury
  2. Elevated (1): cholestasis or liver damage
  3. (1) is a sensitive indicator of hepatic disease, particularly caused by drugs, chemicals, or alcohol
A
  1. ALP has origin in multiple tissues
    • May be normally elevated in late pregnancy, childhood/adolescence
    • Elevation correlates with cholestatic injury
  2. Elevated bilirubin: cholestasis or liver damage
  3. GGT is a sensitive indicator of hepatic disease, particularly caused by drugs, chemicals, or alcohol

ALP high in pregnancy dt high osteoblastic activity -> depositing calcium to help baby’s bones grow

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9
Q

Evaluation of Protein Synthesis

  • Albumin synthesis can be affected by liver disease, dietary pr_____, al____, tr____, and cortico_____
  • Elevated PT/INR may be due to one of these factors or due to Vitamin __ deficit
A
  • Albumin synthesis can be affected by liver disease, dietary protein, alcohol, trauma, and corticosteroids
  • Elevated PT/INR may be due to one of these factors or due to Vitamin K deficit
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10
Q

2. Abnormal LFTs

  1. Will patients always be symptomatic?
  2. Symptoms: an____, mal____, weight ____, pr____
  3. Detailed (1) history
    1. PMH: hepatitis (or symptoms of), abdominal surgery, blood transfusions (before 1992)
  4. Social history: _____ intake
  5. S____ history
  6. Household/work exposure to ch_____
  7. F____ history of liver diseases
A
  1. Patient may be asymptomatic or symptomatic
  2. Symptoms: anorexia, malaise, weight loss, pruritis
  3. Detailed medication history
    1. PMH: hepatitis (or symptoms of), abdominal surgery, blood transfusions (before 1992)
  4. Social history: alcohol intake
  5. Sexual history
  6. Household/work exposure to chemicals
  7. Family history of liver diseases
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11
Q

Physical Exam

Findings present only probably with significant damage

  • Sclera (1)
  • Skin exam (3)
  • Abdominal exam (4)
  • Neuro exam (1)
A
  • Icterus
  • Spider angioma, palmar erythema, jaundice
  • Ascites, RUQ tenderness, hepatomegaly, splenomegaly
  • Asterixis
  • Asterixis = twitching of fingers when they hold their hands in front of them - asctd with elevation of ammonia*
  • Elevated ammonia -> day night reversal, memory impairment, confusion (asctd with end stage liver disease)*
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12
Q

Diagnostics/Labs

  • _____ function panel
  • This includes (2)
  • C___ does not include ggt
  • C__ w/diff
A
  • Liver function panel
  • This includes ggt, bilirubin
  • CMP does not include ggt
  • CBC w/diff
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13
Q

Hepatitis Panel

Hep A (1)

Hep B (3)

Hep C (1)

A
  1. Hepatitis A Ab total
  2. Hepatitis B s ab
  3. Hepatitis B s ag with reflex
  4. Hepatitis B core ab total
  5. Hepatitis C ab with reflex to HCV RNA
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14
Q

Hepatitis A Ab total

=

can you vaccinate?

A

Hepatitis A Antibody

Have they ever had hepatitis and is immune? (hep A antibody total) -> if negative some labs will automatically reflex - can vaccinate for Hep A but no vaccine for Hep C

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15
Q

Hepatitis B Labs

What does each value mean?

  1. Hepatitis B s ab =
  2. Hepatitis B core ab total =
  3. Hepatitis B s ag with reflex =
  • If positive surface antibody and core antibody =
  • If positive surface antibody and negative core antibody =
A
  1. Hepatitis B s ab = IMMUNITY through vaccination or past infection (we want this to be positive)
  2. Hepatitis B core ab total = EXPOSURE to Hep B (kind of like the IgM of
  3. Hepatitis B s ag with reflex = CURRENTLY REPLICATING/ACTIVE INFECTION (AG = actively growing)
  • If positive surface antibody and core antibody = had a past infection that cleared and has immunity
  • If positive surface antibody and negative core antibody = passive immunity from vaccine
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16
Q

Investigation of Abnormal LFTs

Additional tests to investigate why liver enzymes are elevated, what are we looking for?

(2) (3), (5)

A

Looking for autoimmune disease

Immunoglobulins

  1. IgG
  2. IgM
  3. IgA

Autoantibodies

  1. ANA (anti-nuclear)
  2. A-SM (anti-smooth muscle)
  3. A-LKM (ant-liver/kidney microsomal)
  4. AMA (anti-mitochondrial)
  5. P-ANCA (antineutrophil cytoplasmic)
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17
Q

Immunoglobulins + Abnormal LFTs

  1. IgG can indicate (1)
  2. IgM can indicate (1)
  3. IgA can indicate (1)
A
  1. IgG = Autoimmune hepatitis
  2. IgM = Primary biliary cirrhosis (PBC)
  3. IgA can indicate = alcohol
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18
Q

Auto-Antibodies + Abnormal LFTs

  1. ANA (anti nuclear) (3)
  2. A-SM (anti-smooth muscle) (2)
  3. A-LKM (anti-liver/kidney microsomal) (1)
  4. AMA (anti mitochondrial) (1)
  5. P-ANCA (antineutrophil cytoplasmic) (1)
A
  1. ANA (anti nuclear)-AIH, primary sclerosing cholangitis (PSC), PBC - bc ANA is non-specific
  2. A-SM (anti-smooth muscle)-AIH, PSC
  3. A-LKM (anti-liver/kidney microsomal) – AIH
  4. AMA (anti mitochondrial) – PBC
  5. P-ANCA (antineutrophil cytoplasmic)- PSC

P-ANCA also asctd with chron’s and colitis

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19
Q

Hemochromatosis

=

Labs to check

  • Iron labs (1)
  • Consider human (1) genotype
A

Genetic condition where you have iron overload and iron gets deposited in liver and causes inflammation and damage

  • Ferritin, Transferrin saturation
  • HFE (human homeostatic iron regulator protein)
  • hemochromatosis + statin example of a synergistic combo -> 1+1 = 4*
  • Tx for hemochromatosis = blood removal/transfusion*
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20
Q

Hemachromatosis Labs

  • Normal Ferritin levels
    • < ___ ugm/l for males and
    • < ___ ugm/l for females
  • Fe sat = fe/tibc x 100 (normal < ___%)
  • Investigate when saturation > __-__%
  • Fasting fe > ____ ugm/dl suggests true abnormality
A
  • Normal Ferritin levels
    • < 300 ugm/l for males and
    • < 200 ugm/l for females
  • Fe sat = fe/tibc x 100 (normal < 33%)
  • Investigate when saturation > 50-_55%
  • Fasting fe > 175 ugm/dl suggests true abnormality
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21
Q

Hemachromatosis Genetic Predisposition

(2) genetic defects

1 or both gene mutations is present in 85-95% of pts with genetic hemochromatosis and 5% without

_____ zygotes may have some degree of iron overload

A

C282y and h63d genetic defects

1 or both gene mutations is present in 85-95% of pts with genetic hemochromatosis and 5% without

heterozygotes may have some degree of iron overload

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22
Q

Wilson’s Disease

=

What lab value do we check if we are suspecting this disease? What does it do?

A

Genetic autosomal recessive condition that leads to impairment of cellular copper transport resulting in copper accumulation in liver, brain, cornea

Low Ceruloplasmin

Ceruloplasmin is the major carrier of copper in the blood and an important enzyme with ferroxidase activity. Ceruloplasmin is synthesized by hepatocytes and secreted in the blood

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23
Q

Wilson’s Disease S/S

(1)*

  • Over time liver damaged, becomes _____
  • Majority of patients diagnosed between ages __-__
  • H____, n_____ and ps_____ clinical manifestations
  • Hemo____ common finding
  • Imaging (1)
A

Kayser-Fleischer rings

(visible in 50% patients), dark (brown) rings that appear to encircle the iris of the eye

  • Over time liver damaged, becomes cirrhotic
  • Majority of patients diagnosed between ages 5-35
  • Hepatic, neurologic and psychiatric clinical manifestations
  • Hemolysis common finding
  • Imaging- US

(suspect in young patients with headaches, behavioral issue (that doesn’t rly match ADHD)

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24
Q

Alpha 1 Anti-Trypsin Deficiency

=

Results from _____ within the hepatocyte of un secreted variant (1)

(1) lab value to check

A

Inherited disorder affecting lungs, liver (and rarely skin)

Results from accumulation within the hepatocyte of un secreted variant AAT protein

Alpha 1 Anti-Trypsin level

  • Autosomal co dominant transmission (complicated genetic profile-over 150 allelic variants)
  • “Toxic gain of function”
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25
Approach to Elevated Liver Function Tests
26
Radiology (5)
**Abdominal Ultrasound** **HIDA (Hepatobiliary Iminodiacetic Acid Scan)** **CT** **Magnetic Resonance Cholangiopanreatography (MRCP)** **Endoscopic retrograde cholangiopancreatography (ERCP)** Abdominal ultrasound: may detect obstruction, not fully reliable-may have contracted gallbladder but the presence of common bile duct stones ERCP can remove stones or place a stent
27
Caveats * Abnormal LFTs do not always ______ liver disease…… * Normal LFTs do not always ______ liver disease……. * (1) virus – 1 out of 6 patients with persistently normal ALT will have significant pathology on liver biopsy * Clear link between (1) elevation and liver mortality, even for values within the normal range * In a community setting \>70% with abnormal imaging (fibrosis on US) had _____ LFTs
* Abnormal LFTs do not always indicate liver disease…… * Normal LFTs do not always exclude liver disease……. * HCV – 1 out of 6 patients with persistently normal ALT will have significant pathology on liver biopsy * Clear link between ALT elevation and liver mortality, even for values within the normal range * In a community setting \>70% with abnormal imaging (fibrosis on US) had normal LFTs *(End stage cirrhosis will show normal LFTs bc their hepatocytes are NOT working)*
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Differential Diagnosis 1. **Elevated ALT and AST** * al\_\_\_\_ or v\_\_\_\_ hepatitis; cyto\_\_\_\_ drugs, NASH = /NAFLD = 2. **Elevated Alkaline Phosphatase** * ob\_\_\_\_\_ of (1) system * intrahepatic: med\_\_\_\_ or inf\_\_\_\_\_ * extrahepatic: gall\_\_\_\_\_ 3. **Elevated Bilirubin** * may be elevated in hep\_\_\_\_
1. **Elevated ALT and AST** * alcoholic or viral hepatitis; cytotoxic drugs, NASH/ NAFLD (non-alcoholic steatohepatitis-fatty liver disease) 2. **Elevated Alkaline Phosphatase** * obstruction of biliary system * intrahepatic: medications or infiltrative * extrahepatic: gallstones 3. **Elevated Bilirubin** * may be elevated in hepatitis
29
Plan * First step is d\_\_\_\_\_\_ testing * If no underlying cause is found and patient is asymptomatic, **\_\_\_\_\_\_ ~\_-\_ months for progressive symptoms and liver dysfunction** * Do further lab testing with **(1) panel and consider (1)** imaging; if abnormal-consult with a **(1)**
* First step is diagnostic testing * If no underlying cause is found and patient is asymptomatic, observe ~1-3 months for progressive symptoms and liver dysfunction * Do further lab testing with ***hepatitis panel*** **and consider ultrasound**; if abnormal-consult with a **specialist** * hepatitis panel + US (if pt is large may need CT/MRI)* * still no findings, specialist will probably want to get a liver biopsy*
30
Therapeutic Recommendations 1. Eating recommendation = 2. Prohibit use of **(2)** 3. Avoid **sed\_\_\_\_\_** 4. Monitor **P\_\_**, serum **al\_\_\_\_\_**, and **b\_\_\_\_\_** 5. Daily **(1);** regular **hem\_\_\_\_\_** testing 6. Check for signs of **(1)** *CNS* at each visit 7. Check abdomen for signs of **(1)**
1. Maintain **normal caloric intake** 2. **Prohibit** use of **alcohol or hepatotoxic agents** *(ie tylenol)* 3. Avoid **sedatives** 4. Monitor **PT,** serum **albumin**, and **bilirubin** 5. Daily **weights**; regular **hemoccult** testing 6. Check for signs of **encephalopathy** at each visit 7. Check abdomen for signs of **ascites**
31
3. _Chronic Liver Disease_ **Causes of Chronic Liver Disease** 1. Al\_\_\_\_\_ 2. V\_\_\_\_\_ 3. Non-alcoholic ____ liver disease 4. Immunological (3) 5. Genetic / Metabolic (3)
1. Alcohol 2. Viral 3. Non-alcoholic fatty liver disease *(NAFLD or NASH)* 4. Immunological 1. Autoimmune hepatitis 2. Primary sclerosing cholangitis 3. Primary biliary cirrhosis 5. Genetic / Metabolic 1. Hereditary hemochromatosis 2. Wilson’s disease 3. Alpha 1- antitrypsin deficiency
32
Liver Disease Severity * Biochemical (3) labs * Clinical presentation (3)
* Biochemical * Albumin * PT * Bilirubin * Clinical * Ascites * Hepatic encephalopathy * Nutritional status
33
Jaundice or Icterus * **Pre-hepatic Causes =** * **Hepatic Causes =** * **Post-hepatic Causes =**
* **Pre-hepatic Causes** = Disorders that cause hemolysis and lead to excessive bilirubin levels * **Hepatic Causes** = Hepatic injury * **Post-hepatic Causes** = Obstructions of bile ducts
34
History: Jaundice * **Abdominal (1)**: obstruction * **Skin (1)**: indicates biliary obstruction * **Easy (1) on skin**: due to splenomegaly secondary to portal (1) or alcohol secondary to dietary insufficiency- inadequate vitamin (1) * Alcoholism, exposure to hepatitis (A, B, C, D, E), flu-like prodrome, hepatocellular disease risk factors * **(1) urine, (1) stools:** conjugated bilirubinemia * **Hx gall\_\_\_\_, sur\_\_\_, f\_\_\_\_**: obstruction * **Meds causing cholestasis**: est\_\_\_\_\_\_, pheno\_\_\_\_
* **Abdominal pain**: obstruction * **Pruritis**: indicates biliary obstruction * **Easy bruising**: due to splenomegaly secondary to portal hypertension or alcohol secondary to dietary insufficiency- inadequate vitamin K * Alcoholism, exposure to hepatitis (A, B, C, D, E), flu-like prodrome, hepatocellular disease risk factors * **Dark urine, pale stools:** conjugated bilirubinemia * **Hx gallstones, surgery, fever**: obstruction * **Meds causing cholestasis**: estrogens, phenothiazides
35
Physical Exam 1. Focus on signs of liver disease other than jaundice, including * Skin (3) * Chest (1) * Testes (1) * Abdomen (1) 2. Liver exam * S\_\_\_, f\_\_\_\_ness, t\_\_\_\_\_ of surface, p\_\_\_ * _____ liver indicates advanced hepatocellular disease * **Portal hypertension**: (1)megaly, prominent abdominal v\_\_\_\_\_pattern, as\_\_\_\_ * **(1)** enlarged-inflamed/ obstructed 3. Splenomegaly * may be hemo\_\_\_\_ disease
1. Focus on signs of liver disease other than jaundice, including * Skin = brusing, spider angiomas, palmar erythema * Chest = gynecomastia * Testes = testicular atrophy * Abdomen = presence or absence of ascites also should be noted 2. Liver exam * Size, firmness, texture of surface, pain * Small liver indicates advanced hepatocellular disease * Portal hypertension: splenomegaly, prominent abdominal venous pattern, ascites * Gallbladder enlarged-inflamed/ obstructed 3. Splenomegaly may be hemolytic disease
36
Diagnostics for Chronic Liver Disease * L\_\_\_\_ * (1) with diff and platelets * Coags (2) * H\_\_\_\_\_ profile * C\_\_\_\_ * Iron panel (3)
* LFTs * CBC with diff and platelets * PT/PTT *(pt/inr ratio included)* * Hepatitis profile * CMP * Serum iron, ferritin, transferrin saturation
37
Additional Diagnostics to Consider in Chronic Liver Disease * Serum cer\_\_\_\_\_\_ * Anti\_\_\_\_\_ antibodies (AMA) * Anti-\_\_\_\_\_\_ antibodies (ANA) * Anti-\_\_\_ _____ Antibodies (ASMA) * Anti-l\_\_\_\_ k\_\_\_\_ microsomal (Anti-LKM) * ___ anti\_\_\_\_\_activity * (1) disease screening included
* Serum ceruloplasmin * Antimitochondrial antibodies (AMA) * Anti-nuclear antibodies (ANA) * Anti-Smooth Muscle Antibodies (ASMA) * Anti-liver kidney microsomal (Anti-LKM) * α 1 antitrypsin activity * (HIV screening included)
38
Chronic Liver Disease Imaging * U\_\_\_\_\_\_ * C\_\_\_ scan * E\_ _ *\_* * M _ \_ \_ * En\_\_\_\_\_ ultrasonography * Liver b\_\_\_\_\_
* Ultrasound * CT scan * Endoscopic retrograde cholangiopancreatograpy * Magnetic resonance cholangiopancreatography * Endoscopic ultrasonography * Liver biopsy
39
4. _Jaundice Management_ 1. Treatment of **(1) disease process** 2. **Liver (1)** if LFTs fail to return to normal after 6 months 3. Cholangitis 1. **Anti\_\_\_\_\_, (1) with di\_\_\_\_** 4. Diet 1. **\_\_\_\_ protein (vegetable proteins), ____ sodium, ___ alcohol** 5. Supplements 1. **MVI = , (1) acid**
1. Treatment of underlying disease process 2. Liver biopsy if LFTs fail to return to normal after 6 months 3. Cholangitis *(inflammation of biliary system, most commonly caused by bacterial infection)* 1. Antibiotics, ERCP with dilation 4. Diet 1. High protein (vegetable proteins), low sodium, no alcohol 5. Supplements 1. MVI = multivitamin infusion, folic acid
40
Jaundice Management Continued 1. Avoid barb\_\_\_\_\_ and sed\_\_\_\_ 2. **(1)** Rx- to reduce blood ammonia levels- 20-30G TID-QID 3. **(1) Rx** if encephalopathy worsening on lactulose 4. Pruritis 1. (1) sequesterants- cholestyramine TID 2. Anti-h\_\_\_\_\_\_ 3. Mild s\_\_\_\_ 4. Em\_\_\_\_\_ 5. Liver t\_\_\_\_\_\_
1. Avoid barbiturates and sedatives 2. **Lactulose**- to reduce blood ammonia levels- 20-30G TID-QID 3. **Rifaximan** if encephalopathy worsening on lactulose 4. Pruritis 1. Bile acid sequesterants- cholestyramine TID 2. Anti-hystamines 3. Mild soaps 4. Emollients 5. Liver transplant *bile acid sequestrants -be careful bc can cause constipation - want them to stool to excrete the ammonia*
41
_5. Hepatitis_ = Causes (3), (2) diseases
**Inflammation of the liver** Alcohol Viruses Medications Autoimmune diseases Metabolic diseases
42
Medication Induced Hepatitis Common medications that cause hepatitis 1. Ac\_\_\_\_\_\_ 2. All\_\_\_\_\_\_\_ 3. High dose as\_\_\_ 4. Capto\_\_\_\_ 5. Carb\_\_\_\_\_\_\_ 6. Iso\_\_\_\_\_\_ 7. Keta\_\_\_\_\_\_ 8. Methyl\_\_\_\_ 9. NS\_\_\_\_\_ 10. Pro\_\_\_\_\_\_ 11. Sulf\_\_\_\_\_\_
1. Acetaminophen 2. Allopurinol 3. High dose aspirin 4. Captopril 5. Carbamazepine 6. Isoniazid 7. Ketaconazole 8. Methyldopa 9. NSAIDs 10. Procainamide 11. Sulfonamides
43
Viral Hepatitis Stages ## Footnote I II III (3) Sx IV
I Incubation II Prodromal – anorexia, nausea/vomiting, malaise, upper respiratory infection symptoms, myalgia, arthralgia, fatigue, abdominal pain III Icteric – jaundice, dark urine, pale stools IV Convalescent – improved well-being
44
Prevention of Hepatitis Vaccines available for which hepatitis viruses? 1. Hep A vaccine should be given to which children, which adults? 2. Can you give the Hep A vaccine if you have Hep B or C? 3. If a pregnant woman has chronic hepatitis B, the infant should receive (2) 4. Which hepatitis do we not have a vaccine for?
Hepatitis A and B. 1. Hep A vaccine 1. Children 12 to 23 months of age 2. Adults who travel or work in locations with a higher prevalence of hepatitis A infection. 2. Vaccination for hepatitis A also should be given to people with hepatitis B and C. 3. Infant should receive the hepatitis B vaccine as well as hepatitis B immune globulin to prevent the development of chronic hepatitis B. 4. There is no vaccine for hepatitis C
45
Patient Presentation with Viral Hepatitis * Most people are? * An\_\_\_\_, f\_\_\_\_\_, my\_\_\_\_, n\_\_\_\_/ v\_\_\_\_, f\_\_\_, head\_\_\_, arth\_\_\_\_\_, a\_\_\_\_\_\_ pain * Jaundice with Hepatitis \_\_ * Hepatitis B and D clinically in\_\_\_\_\_\_
* Most people are asymptomatic * Anorexia, fatigue, myalgias, nausea/ vomiting, fever, headache, arthralgia, abdominal pain * Jaundice with Hepatitis B * Hepatitis B and D clinically indistinguishable
46
Hepatitis A (1) virus Transmission CDC issues travel advisories that identify what? Eating (1) or (1) foods increases risk for Hep A
RNA virus Fecal oral, person to person, ingestion of contaminated food or water CDC issues travel advisories that identify the countries with outbreaks or endemic hepatitis A Eating raw or uncooked foods increases the risk for hepatitis A
47
Hep A Symptoms * May be * S/S = * When are you infectious? (bimodal) * Can you be a carrier or have chronic hep A?
* May be asymptomatic * Fever, jaundice, anorexia, nausea, malaise, myalgia * Infectious 2 weeks before symptoms and 1 week after * No carrier state or chronic illness
48
Hep A Testing For acute illness = For past infection or immunity = * Does the virus stay in the body after infection? * Over 85% of people with hepatitis A recover within __ months, 99% of patients get better within __ months. * **There are usually __ complications. One in a thousand cases becomes (1), which can be life threatening**
Hep A Ab IgM for acute illness Hep A Ab IgG for past infection or immunity * The virus does not remain in the body after the infection has gone away * Over 85% of people with hepatitis A recover within 3 months, 99% of patients get better within 6 months. * **There are usually no complications. One in a thousand cases becomes fulminant hepatitis, which can be life threatening**
49
Hep A Prevention * Safe (1) * S\_\_\_\_\_\_\_ * V\_\_\_\_\_\_\_ * An\_\_\_\_ handlers * F\_\_\_\_ handlers * \_\_\_\_\_care workers * M\_ \_ * Patients with chronic ___ disease * T\_\_\_\_ abroad * Sew\_\_\_\_ handlers
* Safe water * Sanitation * Vaccination * Animal handlers * Food handlers * Healthcare workers * MSM * Patients with chronic liver disease * Travel abroad * Sewage handlers
50
Hep A Treatment (2)
**Supportive care** **LFTs every 2 weeks until normalize**
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Hepatitis B (1) virus Transmission in Asia/Africa = Transmission in North America and Europe = Hep B outbreaks in 2008-2014 were associated with what?
DNA virus Transmission in Asia and Africa most commonly vertical Transmission in North America and Europe most commonly percutaneous transmission *(through iv drug/ horizontal transmission through sexual contact)* Hepatitis B Outbreaks 2008-2014- 82% were associated with infection control breaks during assisted monitoring of blood glucose
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Hepatitis B Risk Factors * (1) with more than one partner or someone who's infected with HBV * (1) during intravenous (IV) drug use * (1) with someone who has a chronic HBV infection * Have a ____ that exposes you to human blood- related to needle sticks * Receive _______ for end-stage kidney (renal) disease * Travel to regions with high infection rates of HBV, such as (3)
* Unprotected sex with more than one partner or with someone who's infected with HBV * Share needles during intravenous (IV) drug use * Share a household with someone who has a chronic HBV infection * Have a job that exposes you to human blood- related to needle sticks * Receive hemodialysis for end-stage kidney (renal) disease * Travel to regions with high infection rates of HBV, such as Africa, Central and Southeast Asia, and Eastern Europe
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Vaccine Recommendations for Hepatitis B Takeaway =
EVERYONE * All children younger than 18 years, including **newborns**--especially those born to **mothers who are infected with HBV** * All **health care and public safety workers** who may be exposed to bloody people who have hemophilia or other blood clotting disorders and receive **transfusions** of human clotting factors * People who require **hemodialysis** for kidney disease * **Travelers to countries where HBV infection is common** - This includes most areas of Africa, Southeast Asia, China and central Asia, Eastern Europe, the Middle East, the Pacific Islands, and the Amazon River basin of South America. * People who are in **prison** * People who live in **residential facilities f**or developmentally disabled persons * People who **inject illegal drugs** * People with **chronic liver disease** such as hepatitis C * People who have **multiple sex partners** or have ever had a sexually transmitted disease
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Candidates for Screening for HBV Takeaway = * All (1) women * Infants that were (1) * Men who do what (1) * Persons born in high (1) areas (2) * (1) and (1) contacts of HBsAg+ ppl * Ppl who have ever injected (1) * Ppl with multiple (1) or hx of STDs * (1) of correctional facilities * Ppl with chronically elevated (1) * Ppl infected with (2) * Patients undergoing (1)
EVERYONE
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Acute vs. Chronic Hepatitis B Serology What is the main difference in Hep B serologies in acute vs. chronic infection?
In chronic infection the patient is still making virus so Hep B antigen and DNA will still be elevated
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Acute Hep B Infection What are the levels for each phase Early phase? Window phase? Recovery phase? 1. HbsAg = 2. IgM = 3. total anti-Hbc = 4. Anti-Hbs = 5. HBV DNA 6. ALT
Surface antigen = active replication of virus IgM = acute Core antibody = every been exposed Anti-HBs = surface antibody (IMMUNITY) *HBeAg goes along with surface antigen*
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What do these values mean?
Acutely Infected
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Chronic Hep B Infection Phases HBsAg-positive for \> __ months (5) phases
HBsAg-positive for \> 6 months 1. **Immune- Tolerant Phase** 2. **Immune-active HBeAg Positive** 3. **Immune-active HBeAg Negative** 4. **Inactive chronic HBV** 5. **Occult HBV** *most patients will however go to chronic states where their surface antigen will be elevated for about ~6m*
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Chronic Hep B Immune-Tolerant Phase 1. HBsAg = 2. HBeAg = 3. Total anti-HBc = 4. Anti-HBs = 5. HBV DNA = 6. ALT =
1. HBsAg = Positive 2. HBeAg = Positive 3. Total anti-HBc =Positive 4. Anti-HBs = Negative 5. HBV DNA = \>1 million 6. ALT = Normal or mildly elevated
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Chronic Hep B Immune-Active HBeAg-positive Phase 1. HBsAg = 2. HBeAg = 3. Total anti-HBc = 4. Anti-HBs = 5. HBV DNA = 6. ALT =
1. HBsAg = Positive 2. HBeAg = Positive 3. Total anti-HBc = Positive 4. Anti-HBs =Negative 5. HBV DNA = \>20,000 6. ALT = persistently elevated
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Chronic Hep B Immune-Active HBeAg-negative Phase 1. HBsAg = 2. HBeAg = 3. Total anti-HBc = 4. Anti-HBs = 5. HBV DNA = 6. ALT =
1. HBsAg = Positive 2. HBeAg = Negative 3. Total anti-HBc = Positive 4. Anti-HBs =Negative 5. HBV DNA = \>2000 6. ALT = Elevated
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Chronic HBV infection Inactive Chronic Phase 1. HBsAg = 2. HBeAg = 3. Total anti-HBc = 4. Anti-HBs = 5. HBV DNA = 6. ALT =
1. HBsAg = Positive 2. HBeAg = Negative 3. Total anti-HBc = Positive 4. Anti-HBs = not measured 5. HBV DNA = _\<_2000 6. ALT = normal or mildly elevated *not enough to be causing liver damage but can still pass to baby*
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Chronic Occult HBV 1. HBsAg = 2. HBeAg = 3. Total anti-HBc = 4. Anti-HBs = 5. HBV DNA = 6. ALT =
1. HBsAg = Negative 2. HBeAg = Negative 3. Total anti-HBc = +/- (generally +) 4. Anti-HBs =+/- 5. HBV DNA = + in liver, - to + in serum 6. ALT = Normal
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What do these values mean?
Susceptible → Vaccinate!
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What do these values mean?
Immune due to natural infection (this is the outcome we want for any pt exposed to Hep B)
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What do these values mean?
Immune due to Hepatitis B vaccination | (Passive immunity)
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What do these values mean?
Chronically Infected → Get viral load
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What do these values mean? (4) possibilities
1. Resolved infection (most common) → repeat surface antibody, monitor viral load 2. False positive anti-HBc, thus susceptible 3. “Low level” chronic infection *(low viral load)* 4. Resolving acute infection (IgM)
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Hepatitis B serologies 1. **HbsAg+ =** 2. **Hbsab+ =** 3. **Hbcab (IGM) =** 4. **Hbcab (IGG)** =
1. **HbsAg+** = active dx or chronic carrier 2. **Hbsab+** =Immunity (passive or previous exposure) 3. **Hbcab (IGM)** = acute exposure 4. **Hbcab (IGG)** = previous exposure
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Hepatitis B Serologies * **Hbeag +** = * **Hbeab +** = * **HBV dna \< 10^5** = * **Hbv dna \> 10^5** =
* **Hbeag +** = acute viral replication * **Hbeab +** = strong viral suppression or pre-core mutant if DNA + * **HBV dna \< 10^5** = chronic carrier or well suppressed * **Hbv dna \> 10^5** = active chronic infection
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Hepatitis B Treatment * **(1)** remains only agent with potential to produce sustained virologic response * Suppressive therapy with nucleoside/nucleotide analogues * \_\_\_fovir, \_\_\_oxovir, \_\_\_vudine, \_\_\_\_citabine, \_\_\_\_citabine, \_\_\_\_cavir, \_\_\_\_vudine, and \_\_\_\_fovir * ________ increase success (adefovir+lamivudine; adefovir+emtricitabine; clevudine+emtricitabine) * Patients coinfected with HIV and HBV recommended treatment with **(1) combo or (1) combo**
* Interferon remains only agent with potential to produce sustained virologic response * Suppressive therapy with nucleoside/nucleotide analogues * Adefovir, amdoxovir, clevudine, elvucitabine, emtricitabine, entecavir, telbivudine, and tenofovir * Combinations increase success (adefovir+lamivudine; adefovir+emtricitabine; clevudine+emtricitabine) * Patients coinfected with HIV and HBV recommended treatment with tenofovir+lamivudine or tenofovir+emtricitabine
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What should you do if a patient comes in and was exposed to Hepatitis B?
**Passive protection from infection by receiving hepatitis B immunoglobulin (HBIG) within 7 days of exposure**
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Hepatitis C What type of Virus? How is it transmitted? Most commonly vertical or horizontal transmission?
Single-stranded RNA genome * There are 6 major genotypes which are indicated numerically and multiple sub-types (~70% genotype 1 in North America) Blood-to-Blood contact Low vertical transmission * Vertical transmission of HCV ~ 6 out of 100 * Hepatitis C Outbreaks 2008-2014- 50% hemodialysis setting * No documented transfusion-related cases of HCV in the US for \> 10years
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Acute Hepatitis C * Incubation \_\_-\_\_ weeks * During acute phase 60-70% HCV positive patients are \_\_\_\_\_\_\_\_\_
* Incubation 6-12 weeks * During acute phase 60-70% HCV positive patients are asymptomatic
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Chronic Hepatitis C Definition = 1. When is Hepatitis C detectable in the blood by PCR? By antibodies? 2. Percent of patients with chronic HCV infection that will develop serious liver disease? 3. What diagnostic test will show the rate of progression of fibrosis or scarring? 4. Factors that influence the rate of HCV disease progression include?
Chronic hepatitis C is defined as infection persisting for **more than six months.** 1. 1-3 wks by PCR, 3-15 wks by antibodies 2. ~20% with HCV infection will develop serious liver disease 3. A liver biopsy 1. Roughly 1/3 of pts progress to cirrhosis (stage 4 fibrosis) in less than 20 years.Another 1/3 progress within 30 years. 4. Increasing age, male gender, alcohol consumption, HIV co-infection and NAFLD
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Hepatitis C Precautions/Transmission * Any recommendations for a change in sexual practice if you are in a long term monogamous relationship with a HCV+ partner? * Can Hepatitis C be spread by hugging, sneezing, or sharing a drinking glass? * What household items should you not share if living with a HCV+ person?
* No change in sexual practice with a HCV+ partner but should use condoms * Hepatitis C is not spread by hugging, sneezing, or sharing a drinking glass * Items that might be contaminated with small amounts of blood, such as razors or nail clippers
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Hepatitis C Screening Who should be screened?
All adults aged 18-79 should be screened for hepatitis C infection
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Hepatitis C Treatment (3) common medications Cost range
Ledipasivir Sofosbuvir Obitasivir 80-190k
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Hepatitis D Type of Virus Requires what for the virus to replicate? Why has HDV transmission decreased in the past 20 years? HBV and HDV co-infection, mortality is?
RNA virus, 8 genotypes Requires co-infection with HBV for replication (maybe transmitted with HBV or super-infected in a patient with HBV) In the past 20 years HDV transmission has decreased because of the HBV vaccine Greater mortality
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Hepatitis E Type of Virus Transmission Most common cause of acute hepatitis in adults in Central and South Eastern (1) Mortality? Except in what patients?
RNA virus with 4 known genotypes Most commonly spread in contaminated water HEV is the most common cause of acute hepatitis in adults in Central and South Eastern Asia Self-limited disease \*\*Infection during pregnancy with HEV leads to liver failure and death especially in third trimester (mortality ~20%)
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Alcoholic Hepatitis * Chronic consumption of excessive alcohol * Women \_\_-\_\_G daily (3-6oz wine, 10-20oz beer, 1-2oz hard liquor) * Men \_\_-\_\_G daily (6-12oz wine, 20-40oz beer, 2-4oz hard liquor) * ~10-35% of heavy drinkers develop * Additional factors that increase risk of alcoholic hepatitis: * G\_\_\_\_\_\_ * En\_\_\_\_\_\_\_ * A\_\_\_ * BMI- men \>\_\_, women \>\_\_
* Chronic consumption of excessive alcohol * Women 10-20G daily (3-6oz wine, 10-20oz beer, 1-2oz hard liquor) * Men 20-40G daily (6-12oz wine, 20-40oz beer, 2-4oz hard liquor) * ~10-35% of heavy drinkers develop * Additional factors that increase risk of alcoholic hepatitis: * Genetics * Environment * Age * BMI- men \>27, women \>25
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Non-Alcoholic Fatty Liver Disease (NAFLD/NASH) = * ____ common chronic liver disease * The most serious NAFLD is (1) * NASH can lead to (1)
* Spectrum of chronic liver diseases associated with metabolic syndrome * Most common chronic liver disease * The most serious NAFLD is Non-Alcoholic Steatohepatitis (NASH) * NASH can lead to cirrhosis
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Drug Induced Liver Injury * Common with **Rx (2)** * ½ of all acute liver failure is caused by hepato\_\_\_\_\_\_ * Possibly _______ predisposition * More than ____ therapeutic agents have been implicated in DILI (Prescriptions, over the counter medications, nutritional supplements, herbal remedies)
* Common with **NSAIDs and antimicrobials** * ½ of all acute liver failure is caused by hepatotoxicity * Possibly genetic predisposition * More than 800 therapeutic agents have been implicated in DILI (Prescriptions, over the counter medications, nutritional supplements, herbal remedies)
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2 Patterns of Drug Induced Liver Injury **(1) Reaction** * Occurs within\_\_ weeks of starting a drug * Example di\_\_\_\_\_ **(1) Reaction** * Can manifest after a ____ of continued usage * Example iso\_\_\_\_\_
* **Allergic reaction** * Occurs within 6 weeks of starting a drug * Example dilantin * **Metabolic reaction** * Can manifest after a year of continued usage * Example isoniazid
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Autoimmune Hepatitis (AIH) * How common is AIH? * Greater incidence in what gender? * ___ ages and ethnicities * Common with other (1) diseases
* Rare * Female \> Male * All ages and ethnicities * Common with other autoimmune diseases
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Autoimmune Liver Disease
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Autoimmune liver Disease Consider once you've? What are some associated autoimmune diseases? Treatment usually requires?
Consider once you've ruled out other causes Crohn's, UC, Sarcoidosis, Hashimoto thyroiditis, Sjogren syndrome, Myositis, Scleroderma Transplantation
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AIH Symptoms * F\_\_\_\_\_ * J\_\_\_\_ pain * GI: N\_\_\_\_, An\_\_\_\_, \_\_\_Q pain * Skin r\_\_\_, J\_\_\_\_\_ * **D\_\_\_\_ urine** * **L\_\_\_\_ stools**
* Fatigue * Joint pain * GI: Nausea, Anorexia, RUQ pain * Skin rashes, Jaundice * **Dark urine** * **Light stools** * Jaundice
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AIH Diagnostics Auto antibodies (3) Indicates most severe disease (1) **Liver (1)\*\***
ANA, SMA (anti-smooth muscle antibody), LKM (Anti liver kideny muscle) SLA (anti-soluble liver antibody), 20% of cases no antibodies present **Liver biopsy**
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AIH Treatment ## Footnote **(1) Rx** **Immune system suppressors (2) Rx** **Eventually (1)**
**Corticosteroids** **Azathioprine or 6 mercaptopurine** **Transplant**
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Types of Biliary Cirrhosis (2)
Primary Sclerosing Cholangitis (PSC) Primary Biliary Cirrhosis (PBC)
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Primary Sclerosing Cholangitis (PSC) = * Leads to **c\_\_\_\_, liver f\_\_\_\_, and hepatocellular \_\_\_\_\_** * ~80% of patients with PSC have (1) other autoimmune disorder * 7 times more common in what gender
**Autoimmune disease of the bile ducts, inflammation, and obstruction both intra- and extra-hepatic** * Leads to **cirrhosis, liver failure, and hepatocellular carcinoma** * ~80% of patients with PSC have Ulcerative Colitis * 7 times more common in men *Alpha fetaprotein - good screening tool for HCC*
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Primary Sclerosing Cholangitis Diagnostics * 80% of patients will have which antibody? **(1)\*** * (2) antibodies + in 20-50% of cases * Diagnostic Imaging (2)
* 80% of patients will have perinuclear anti-neutrophil cytoplasmic antibodies **(P-ANCA)** * ANA and ASMA + in 20-50% of cases * Endoscopic Retrograde Cholangio-Pancreatography * Magnetic Resonance Cholangio-Pancreatography *will often get stents dt strictures*
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PSC Symptoms * F\_\_\_\_\_ * J\_\_\_\_ * Pr\_\_\_\_ * Mal\_\_\_\_\_ * Hepato\_\_\_\_ * Chol\_\_\_\_ * Hepatic en\_\_\_\_\_\_\_
* Fatigue * Jaundice * Pruritis * Malabsorption * Hepatomegaly * Cholangitis * Hepatic encephalopathy
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PSC Treatment (2) surgical interventions (1) Rx to reduce LFTs but has not been shown to improve survivial (1) Rx for Pruritis (1) Rx for episodes of cholangitis Vitamin Supplements (4)
ERCP with dilation Liver transplant *difficult to stent everything so most end up with liver transplant* * Ursodiol- a bile acid reduces LFTs but has not been shown to improve survival * Pruritis- bile acid sequesterants- cholestyramine * Antibiotics for episodes of cholangitis * Vitamin supplements- A, D E, and K
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Primary Biliary Cirrhosis = * 9:1 ____ to _____ ratio, age of diagnosis \_\_**-**\_\_ yo
Slow, progressive destruction of **small bile ducts** in the liver, leads to cholestasis, scarring, fibrosis, and cirrhosis * 9:1 Female to Male ratio, age of diagnosis 30-65
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Primary Biliary Cirrhosis Sx * F\_\_\_\_\_ * J\_\_\_\_\_ * Pr\_\_\_\_ * Xan\_\_\_\_, Xan\_\_\_\_\_ * As\_\_\_\_\_\_ * Spleno\_\_\_\_\_ * Esophageal v\_\_\_\_\_ * Hepatic en\_\_\_\_\_\_\_\_\_\_\_\_
* Fatigue * Jaundice * Pruritis * Xanthoma, Xanthelasma * Ascites * Splenomegaly * Esophageal varices * Hepatic encephalopathy
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PBC Diagnostics 2 antibodies, which one \>90% (3) imaging
\>90% + Anti-Mitochondial Antibodies (AMA), ANA * US * CT scan * ERCP
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PBC Treatment (2) Rx (1) definitive tx Alcohol is \_\_\_\_\_
Ursodiol, Cholestyramine Transplant Alcohol contraindicated * Ursodiol = It can dissolve gallstones when they cannot be removed by surgery. It can also treat primary biliary cirrhosis (PBC), a liver disorder.* * Cholestyramine =* *It can lower high cholesterol levels. It can also treat severe itching caused by liver disease.*
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Cirrhosis = * Best treatment = * Address causes that lead to it: chronic hep\_\_\_\_, chronic al\_\_\_\_ abuse, hemo\_\_\_\_\_\_, primary (1) * Complications include as\_\_\_\_\_, peripheral \_\_\_\_\_, enc\_\_\_\_\_, inf\_\_\_\_, bl\_\_\_\_\_, r\_\_\_\_ dysfunction & el\_\_\_\_ imbalances
**Irreversible stated of chronic liver injury (Stage IV scarring)** * Best treatment is prevention * Address causes that lead to it: * chronic hepatitis, chronic alcohol abuse, hemochromatosis, primary biliary cirrhosis * Complications include ascites, peripheral edema, encephalopathy, infection, bleeding, renal dysfunction, & electrolyte imbalances
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Clinical Presentation with Cirrhosis Subjective * fa\_\_\_\_, easy br\_\_\_\_\_, abdominal s\_\_\_\_, ankle ed\_\_\_ Objective * **Portal (1):** spleno\_\_\_\_\_\_, abdominal dis\_\_\_\_\_-shifting dullness, prominent abdominal v\_\_\_\_ pattern * **chronic failure**: palmar er\_\_\_\_\_, (1) angiomas, par\_\_\_\_ hypertrophy, ____ of pubic or axillary hair, cl\_\_\_\_, gynec\_\_\_\_
Subjective * fatigue, easy bruising, abdominal swelling, ankle edema Objective * portal hypertension: splenomegaly, abdominal distension-shifting dullness, prominent abdominal venous pattern * chronic failure: palmar erythema, spider angiomas, parotid hypertrophy, loss of pubic or axillary hair, clubbing, gynecomastia
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Normal LFT Ranges 1. ALT = 2. AST = 3. ALP = 4. Albumin = 5. Total Protein =
1. ALT = 7-55 U/L 2. AST = 8-48 U/L 3. ALP = 40-129 U/L 4. Albumin = 3.5-5.0 g/dL 5. Total Protein = 6.3-7.9 g/dL
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Normal LFT Ranges 1. Bilirubin = 2. GGT = 3. LD = 4. PT = 5. INR =
1. Bilirubin = 0.1-1.2 mg/dL 2. GGT = 8-61 U/L 3. LD = 122-222 U/L 4. PT = 9.4-12.5 seconds 5. INR = 0.8-1.1
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Case 1 * 19 year old college student who presents to the student health clinic with new onset fatigue, jaundice, pruritis x 3 days * No sig PMH, PSH, FH * Etoh on weekends, 2-3 drinks * Meds: minocycline, multivitamin * No known sick contacts, travel * PE: mild scleral icterus, normal GI exam **You Check Labs** * AST: 180 and ALT 252 * Albumin 4.2, t bili 4.0, alk phos 248 * Hgb/hct 13.1/36, wbc 5.2 k, Plt 210 k * Acute viral hepatitis serologies negative * Do you need more testing? * What is the most likely diagnosis? normal GI exam
Can add GGT Drug induced from minocycline Minocycline is associated with two forms of liver injury; an acute hepatitis-like syndrome that arises within 1-3 months of starting med and chronic hepatitis-like syndrome typically with AIH features * pruritis asctd with bilirubin* * AST ALT elevated* * Albumin normal, bili elevated* * CBC normal*
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Case 2 * 26 year old female grad student was notified by the blood bank she was HBsAg + (she was screened when she went to donate blood). * Liver profile Albumin 4.1, Tbili 0.6, Alk phos 82, ast 18, ALT 22 * Hbsag +, HbcAB +, Hbeag -, HBV DNA 400 IU/mL * What is your diagnosis?
hepatitis B chronic carrier state Defined as: Hbsag+ \>6m, Hbeag -, Hbeab -, Hbv dna \<10^5, persistently normal ast/alt * low DNA \<2000* * Chronic carrier bc very low DNA*
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Case 3 * A 27-year-old woman presents to the urgent care clinic with the new onset of nausea and jaundice. During the past 3 years, she has experienced major problems with drug addiction and has been regularly injecting crystal methamphetamine. She almost always uses clean needles, but 6 weeks ago she shared needles with a man she later found out has hepatitis B virus infection. She has never received HBV vaccine. Two years ago, she had negative antibody tests for hepatitis A, B, and C, but did not return for follow-up and vaccinations. * Her physical examination is normal except for track marks on her arms and visible jaundice. Laboratory studies * Total bilirubin 6.8 mg/dl * Aspartate aminotransferase (AST) 1906 U/L * Alanine aminotransferase (ALT) 2086 U/L * Serology tests for hepatitis A, B, and C viruses are ordered. The panel ordered for hepatitis B includes hepatitis B surface antigen (HBsAg), antibody to hepatitis B surface antigen (anti-HBs), total hepatitis B core antibody (total anti-HBc), hepatitis e antigen (HBeAg), and antibody to hepatitis B e antigen (anti-HBe) * Which of the following serologic profiles would be most consistent with acute HBV infection? * A. HBsAg (-), anti-HBs (+), Total anti-HBc (+), HBeAg (-), anti-HBe (+). * B. HBsAg (+), anti-HBs (-), Total anti-HBc (-), HBeAg (-), anti-HBe (+). * C. HBsAg (+), anti-HBs (-), Total anti-HBc (+), HBeAg (+), anti-HBe (-). * D. HBsAg (-), anti-HBs (+), Total anti-HBc (-), HBeAg (-), anti-HBe (-).
* Which of the following serologic profiles would be most consistent with acute HBV infection? * A. HBsAg (-), anti-HBs (+), Total anti-HBc (+), HBeAg (-), anti-HBe (+). * B. HBsAg (+), anti-HBs (-), Total anti-HBc (-), HBeAg (-), anti-HBe (+). * **_C. HBsAg (+), anti-HBs (-), Total anti-HBc (+), HBeAg (+), anti-HBe (-)._** * D. HBsAg (-), anti-HBs (+), Total anti-HBc (-), HBeAg (-), anti-HBe (-).
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Case 4 * 40 yo patient with a history of dm, obesity, hld comes to see you for medication refill. Labs reveal mildly elevated lfts * Ast 45, alt 70 * Alk phos, tbili, albumin, ggt, hepatitis serologies are negative, alpha 1 antitrypsin level and ceruloplasmin are normal * Abdominal u/s shows increased echogenicity * What is the diagnosis?
fat deposition from increased echogenicity **Fatty liver disease** Tx = control DM, weight loss, statin for HLD, trend LFTs, get baseline PT/INR and albumin, and refer to hepatologist
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Case 5 * A 27 yo female presents with elevated transaminases. She feels well except for general malaise. She drinks alcohol socially. No illicit drug use. Her medical history is significant for acne and hirsutism * Ast 60, alt 85, ggt and t bili normal * What other tests do you want to order? * ANA (it is positive \>1:160) * Anti smooth muscle ab (positive) * Quantitative immunoglobulines show normal IGA and IGM, high IGG * What next? * Diagnosis
AST 60, alt 85, ggt and t bili normal = mild elevation repeat and do hepatitis panel and autoimmune panel Get a liver biopsy Autoimmune Hepatitis
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Case 6 * 21 year old Columbia student presents to your clnic with complaints of nausea, vomiting, diarrhea and anorexia. On pe he has a low grade fever, he is jaundiced and he has RUQ tenderness with palpation * He recently returned from spring break (he went to Mexico) where he drank 8-10 beers daily, ate from street vendor carts * Ast and alt are \> 2000, Tbili 3.5 and alk phos 250 * What are you including in your differential? * What tests do you want to confirm suspected dx?
Differentials * Acute hepatitis A, B, C, D, E, or G * EBV, CMV * Alcoholic hepatitis * Drug induced liver injury What tests? * Repeat transaminases (look at trend - is it going up or down) along with alk phos, albumin, t bili, direct bili, pt/inr * Hep a ab * Hbsag, Hbcag (IGM) * Hep c ab * EBV DNA and CMV DNA * ETOH level if you suspect pt currently intoxicated
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Case 7 * A 34-year-old woman with a history of injecting drug use presents for her first prenatal visit at 10 weeks gestation. She reports use of intravenous and nasal heroin in the past, but states she has been in recovery for seven years and has not used any drugs or alcohol during that time. * She is currently in a monogamous relationship with a man who is the father of her child. She and her partner were both tested about a year ago for HIV when they decided to have children and were found to be HIV negative. She has never been tested for hepatitis B virus (HBV) infection. * Her review of systems is notable for occasional early morning nausea, but is otherwise unremarkable. Her physical examination is normal and fetal heart tones are detected * Which one of the following is the most important step in evaluating this patient with regard to her hepatitis B status? * A. No testing for hepatitis B is indicated since it is highly likely that she received hepatitis B vaccine as a child or as an adolescent. B. No testing for hepatitis B is indicated; begin a three dose series of hepatitis B vaccine * C. Check her serum for hepatitis B surface antibody (HBsAb) * D. Check her serum for antibody to hepatitis B e antigen (anti-HBe)
C. Check her serum for Hepatitis B Surface Antibody (HBsAb)