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Flashcards in GI Disease Deck (72):
1

How do you diagnose acute pancreatitis?

For diagnosis of acute pancreatitis, need 2 of 3:
– Abdominal pain characteristic of disease
– Amylase and/or lipase elevated at least 3x upper limit of normal (ULN)
– Characteristic imaging findings

2

Why is lipase (compared to amylase) often preferred in diagnosing pancreatitis?

• Lipase is preferred: more sensitive and
more specific for acute pancreatitis
• Neither enzyme has accepted prognostic value
• Lipase remains elevated longer than amylase
• Current recommendations are for lipase measurement alone.

3

How does sensitivity/specifity compare for diagnosis of pancreatitis w/ lipase and amylase?

Lipase: 90/93
Amylase: 78/92

4

What else besides acute pancreatitis can cause elevations in pancreatic enzymes?

•Macroamylasemia/macrolipasemia
• Renal failure
• Acute appendicitis
• Cholecystitis
• Intestinal ischemia or obstruction
• Peptic ulcer disease
• Gynecological disease
• Diabetes (higher lipase, so diagnostic cutoff is >3-5 ULN, but no consensus on actual value)
• Parotid/salivary gland disease (amylase only)

5

What are causes of acute pancreatitis?

• Gallstones and alcohol are most common
• Hypercalcemia, hypertriglyceridemia
• Post-ERCP, trauma/injury
•Genetic pancreatitis(e.g.,CFmutations)
• Drugs (e.g., azathioprine, sulfonamides, NSAIDs, steroid, tetracycline)
• Viral infections (e.g., mumps, rubella, EBV, CMV, hepatitis)

6

bruising around umbiliccus

cullens

7

bruising around spleen/flank

greys

8

What are first tier LFTs?

• Transaminases
– ALT, AST
• Bilirubin
• Alkaline phosphatase, γ-glutamyl transferase (GGT)
• Albumin
• Prothrombin time/INR

9

What are second tier LFTs?

• Hepatitis viral serologies and molecular
tests
• Fe, ferritin, Cu
• Alpha-1 antitrypsin
• Autoantibody tests

10

What are the three classifiaitons of liver disease?

1. hepatocellular injury/necrosis (damage/death to hepatocytes)
ALT,AST > AP

2. Cholestatic (obstruction of bile outflow from liver)
AP > ALT or AST

3. Infiltrative (neoplasm, amyloid)
elevated AP w/ normal ALT, AST or AP > ALT, AST

11

What are transaminases and how do they differ?

• ALanine aminotransferase (ALT) (SGPT)
• ASpartate aminotransferase (AST) (SGOT)
• These “leak” from damaged hepatocytes
• ALT is more SPECIFIC for LIVER disease
– AST is found in MUSCLE and RED
– With extensive muscle breakdown, both ALT and AST rise
• ALT has a LONGER half-life

12

Where does AP come from?

• Present on hepatocyte membrane
bordering the bile canaliculi
• Isoenzymes: liver, bone, placenta
– Elevation is not a specific marker for liver disease
• Bone, GI, kidney

13

When would you order GGT?

to confirm a liver source

14

What are reference intervals for AST/ALT?

• AST 0-45 U/L, female; 0-55 U/L, male
– Children higher to age 2
• ALT 0-50 U/L, female; 0-70 U/L, male

15

What are reference intervals for AP?

• Alkaline phosphatase 40-150 U/L

16

What are markers of liver function?

• Albumin
– Half-life of 21 days, but can fall more rapidly with severe inflammation
– Can fall with renal or GI losses, or burns
• Prothrombin time (PT, INR)

17

What causes an acute rise in transaminases?

HepA/B
Drug induced hepatitis
Alcoholic
Ischemic (shock liver)
Acute duct obstruction
Wilson disease
Autoimmune hepatitis

18

Diagnostic test: Hep A

IgM anti-HAV

19

Diagnostic test: Hep B

HBsAg, IgM angti-HBc

20

Diagnostic test: drug induced hepatitis

improvement on stopping

21

Diagnostic test: alcoholic

liver bx
improvement iwth abstinence
AST:ALT >2
AST <400

22

Diagnostic test: shock liver

improvement iwth restoration of circulation

23

Diagnostic test: acute duct obstruction

cholangiography

24

Diagnostic test: wilson disease

ceruloplasmin
urine copper
slit lamp
liver Cu measurement

25

Diagnostic test: autoimmune hepatitis

anti-smooth muscle (f actin)
anti-LKM type 1

26

How high can ALTL be with acute hepatitis?

thousands

27

If ALT over 5000 consider....

acetaminophen
hepatic ischemia
unusual viruses like HSV

28

stones can cause transient elevations to...

1000s

29

alcoholic hepatitis cuases modest elevations to...

less than 400 (bili is often elevated more)

30

What are common cuases of chronic hepatitis?

HepC/B (anti-HCV, RNA, HBsAg)
NASH (US, liver bx)
Alscoholic liver disease (liver bx)

31

How do you define chronic hepatitis?

>3 mos
transaminases usually 205 fold elevated
pt can be asymptomatic

32

what characterizes cholestatic disrorders?

rise in AP and bili

33

blockage of microscopic ducts

primary biliary cholangitis

34

blockage of large ducts

obstruction
ca of head of pancreeas
stones

35

blockage of large and small dcuts

primary sclerosing cholangitis

36

What are common causes of cholestasis?

PBC
PSC
Large bile duct obstruction
drug induced
infiltrative/malignancy
inflammation

37

Middle-aged women
Anti-mitochondrial antibody

Primary biliary cholangitis

38

Usually men 20-50; ulcerative colitis
Cholangiography

primary sclerosing cholangitis

39

Jaundice, pain
Ultrasound

large bile duct obstruction (stone, tumor)

40

Malignancy, sarcoid, amyloid
Ultrasound, CT

drug induced

41

adult bili ref range

.2 - 1.3

42

first 2 wks of life bili

0-11.7

43

bilirubinuria is = ...

lier disease

44

>85%
insoluble, carried by albumin
elevation means hemolysis

unconjugated/indirect

45

<15%
soluble
elevations mean liver disease (parenchyma/biliary tract)

conjugated/direct

46

When is jaundice visible?

bili > 2.5 mg/dL

47

What causes unconjugated hyperbilirubinemia?

• Hemolysis, resorption of a large hematoma,
ineffective erythropoiesis (e.g., B12 deficiency)
• Neonatal physiologic hyperbilirubinemia
• Gilbert syndrome

48

What is Gilbert syndrome?

– Benign defect in UDPGT activity
– 3-7% of the population, M:F 2-7:1
– Manifests in stress conditions, including fasting – Bilirubin < 6.0 mg/dL
– LFTs normal, Hb normal
– No treatment, just reassurance

49

What suggests conjugated hyperbijjlirubinemia?

– Suggested by abdominal pain, fever, palpable gall bladder
– Ultrasound reveals duct dilation, unless very transient (e.g., passage of a gall stone)
– A transient rise in aminotransferase levels can be seen with acute large duct obstruction

50

alcoholic hepatitis

• Hepatocellular injury
• AST> 2xALT, but AST <400UL
• Bilirubin increase and PT/INR better indices

51

What viruses classically cuase viral hepatitis?

Hep A, B (D,C,E)
CMV
EBV
HSV

52

What should you exclude before diagnosing autoimmune hepatitis?

chronic viral hepatitis
wilson disease

assoc w/ Hashimotos thyroiditis

53

WHat is primary biliary cirrhosis?

• Typically middle aged women (40-60 yrs)
• Presents with fatigue and pruritus
• Increased levels of AP and IgM
• Fat soluble vitamin deficiencies and metabolic bone disease, increased cholesterol (HDL), later increased bilirubin
• Granulomatous infiltration of septal bile ducts
• Anti-mitochondrial antibodies present in over 90-95%

54

Autoimmune hepatitis vs PBC

Autoimmune hepatitis:
7-10x ULN
anti-smooth muscle Ab 90%

PBC:
1-3xULN
anti-mito 90-100%

55

What causes toxic hepatitis?

• Alcohol
• Drugs
– Predictable (e.g., acetaminophen) – Idiosyncratic (e.g., isoniazid)
• Environmental
– Vinyl chloride
– Jamaica bush tea
– Kava kava
– Amanita phalloides or A. verna (mushrooms)

56

acetaminophen toxicity: 0-24 hrs

Anorexia, nausea, vomiting

57

acetaminophen toxicity: 24-72

Right upper quadrant abdominal pain (common)
AST, ALT, and, if poisoning is severe, bilirubin and PT (usually reported as the INR) sometimes elevated

58

acetaminophen toxicity: 72-96

Vomiting and symptoms of liver failure Peaking of AST, ALT, bilirubin, and INR Sometimes renal failure and pancreatitis

59

acetaminophen toxicity: >5

Resolution of hepatotoxicity or progression to multiple organ failure (sometimes fatal)

60

What is hte rumack matthew nomogram

Hours vs. Plasma acetaminophen (can determine if hepatotoxicity likely given level and how many hours out)

61

What causes Fe overload?

Herediatary hemochromatosis
Multiple blood transfusions (talassemia major)
Consider in adults w/ liver disease (men)

62

What should you consider in a pt with transferrin saturation >55% and ferritin > 200?

Fe overload

Liver bx with Fe measurement

63

Where does Cu accumulate in wilsons disease?

liver
basal ganglia

64

defect in wilson disease

ATP7B gene (increased Cu absorption, decreased excretion)

65

What are sxs of Wilson diesase?

• Hepatitis, splenomegaly, hypersplenism, Coombs neg. hemolytic anemia, portal hypertension, neuro-psychiatric disease
• Can cause chronic or fulminant hepatitis
• Kayser-Fleischer ring seen on slit-lamp exam

66

Wilson disease is usually diagnosed in what population?

adolescent or young adult

67

Labs diagnostic of WIlsons?

• Increased urinary Cu (> 40 μg/24 h)
• Low serum ceruloplasmin (<20 mg/dL; <5 mg/dL is diagnostic) (Cu binding protein)
• Increased hepatic Cu (>250 μg/g dry wt.)

68

What is Crigler Najjar type 1?

• Very rare, newborns
• Unconjugated hyperbilirubinemia
• Bilirubin > 20 mg/dL
• Fatal disease, kernicterus – Liver transplant
• ABSENT UDPGT activity

69

What is Crigler Najjar type 2?

• More common than type 1
• Unconjugated hyperbilirubinemia • Can survive to adulthood
• Bilirubin 5-25 mg/dL
• Milder DEFICIENCY of UDPGT
– Enzyme can be induced by phenobarbital

70

What are dubin johnson and rotor syndromes?

• Both are rare, benign disorders with asymptomatic jaundice
• Often present in 2nd decade of life
• Increased direct (conjugated bilirubin)
• Dubin-Johnson caused by mutations in multiple drug resistance protein 2
• Rotor syndrome mechanism unclear

71

Neonatal jaundice affects what % of newborns?

60%

acute encephalopathy > kernicterus

72

What causes neonatal jaundice

• Usually immaturity of conjugating enzymes
• Other causes
– Hemolytic disease (incl. HDN), bruising (e.g.,
cephalohematoma)
– Breast feeding, especially if inadequate – Sepsis