GI Flashcards

1
Q

Patient presents with jaundice, RUQ pain, n/v/d, what common medication do you need to ask about?

A

tylenol!

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2
Q

Patient has elevated liver enzymes (in the low 100’s, not crazy high), what social history questions are important? (4)

A
  • chronic alcohol abuse
  • injection drug use
  • sexual promiscuity
  • travel to countries with endemic parasitic liver
    diseases. .. (not sure what these are)
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3
Q

Liver enzymes are elevated, patient is mildly itchy, suspect cholestasis due to liver dysfunction, what might happen to the colour of their stool and urine?

A

Cholestasis causes white (acholic) stools and brown or tea-colored urine

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4
Q

PHYSICAL EXAM findings of liver failure?
acute hepatitis (1)
chronic liver disease (9)

A
  1. Hepatomegaly and tenderness +/- jaundice
  2. Chronic liver disease
    - jaundiced complexion
    - extremity muscle atrophy/weight loss
    - easy bruising or signs of easy bleeding
    - Dupuytren’s contracture
    - palmar erythema
    - cutaneous spider nevi
    - distended abdomen with a fluid wave
    - enlarged veins on the surface of the abdomen (caput medusae)
    - asterixis
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5
Q

Two markers/tests of hepatic synthetic function?

A

prothrombin time and albumin

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6
Q

ALT in what approximate ballpark?

  • Mild hepatocyte injury or smouldering inflammation…
  • Acute hepatic necrosis (acute viral or acute toxicity)…
A

Elevations in the hundreds of units per liter suggest mild injury, or smoldering inflammation.

Levels in the thousands suggest extensive acute hepatic necrosis.

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7
Q

What ballpark ALT levels would be more likely alcoholic or fatty liver disease? (hint: how many times normal)

A

Less significant elevations, less than five times normal, are typical of alcoholic liver disease and nonalcoholic steatohepatitis

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8
Q

What AST to ALT ratio do you expect in alcoholic hepatitis?

A

An AST–to–ALT ratio of greater than 2 is common in alcoholic hepatitis because alcohol stimulates aspartate aminotransferase production.

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9
Q

your patient is diabetic and obese, their liver enzymes are elevated, what is tolerable elevations that might be expected in NAFLD?
ALT?
ALP?

A
  • transaminase elevations of three to five times normal

- alkaline phosphatase of up to twice normal

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10
Q

What cause does an elevated GGT in the setting of hepatitis suggest?

A

alcoholic cause

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11
Q

ALT is normal, but ALP and bili are more elevated, what genre of pathology does this suggest?

A
  • biliary obstruction, cholestasis

Mild to moderate elevations of ALP accompany virtually all hepatobiliary disease, whereas elevations greater than four times normal strongly suggest cholestasis.

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12
Q

Where else does ALP come from? (4 big ones)

A

Alkaline phosphatase is a nonspecific marker, hepatic, but also derived from bone, placenta, malignancy

… also intestine, kidneys, and leukocytes. A level of up to double the expected value is normal in pregnancy

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13
Q

What is a pre-hepatic cause of elevated bili?

hint: what is bili derived from?

A

hemolysis

derived from heme breakdown

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14
Q

You wonder if the elevated bili could be from hemolysis, what test do you order?

A

LDH

Hemolysis can produce elevation of lactate dehydrogenase and unconjugated bilirubin.

Lactate dehydrogenase (LDH) is a nonspecific marker. Moderate elevations are seen in all hepatocellular disorders and cirrhosis, whereas purely
cholestatic conditions cause minimal elevations.
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15
Q

What coagulation factors does the liver produce/ synthesize?

Hint: these are also the ones affected by warfarin

A

vitamin K–dependent coagulation factors II, VII, IX, and X

remember 1972 = 10, 9, 7, 2

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16
Q

What happens first with liver dysfunction, prolonged PTT/INR or low albumin?

Most common other cause of low albumin?

A

PTT in days, albumin in weeks
Low albumin in malnutrition

  • PRR becomes prolonged in a matter of days.
  • Albumin half-life is approximately 3 weeks
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17
Q

What do you order for the hep A, B,C serologies…

A

hep A virus antibody
hep B virus surface antigen
hep B virus core antibody
hep C virus antibody (6-8 week delay between infection and antibody detection)

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18
Q

Typical presentation of acute hepatitis on history?

A
  • nausea, vomiting, and RUQ pain
19
Q

What might you see on urine dip in the context of ?hepatitis

hint: didn’t realize this was on a urine dip… if significant may just notice visually

A

Bilirubinuria - bili in urine, dark urine, marker of conjugated hyperbilirubinemia (hepatic or post-hepatic) and can be the earliest sign of hepatic or biliary disease

20
Q

How is hep A transmitted?

A

Hepatitis A virus is transmitted by fecal–oral contamination

21
Q

Incubation period of Hep A virus

A

Hepatitis A virus infection has an incubation period of about 2 weeks to 2 months

Typical course

  • Prodrome of nausea, vomiting, malaise
  • About a week into the illness, patients may note dark urine (bilirubinuria)
  • A few days later, they develop clay-colored stools and jaundice
  • No chronic component
22
Q

How is hep B virus transmitted? (3)

A
  • sexually
  • blood (transfusion, contaminated needles)
  • perinatal (“vertical”)
23
Q

What population is most likely to develop chronic hep B?

A

Acute to Chronic Hep C

  • 90% if infected in infancy
  • 30% if infected <5 yo
  • 6-10% of adults

**underlines the importance of vaccination of infants and women of childbearing age

24
Q

If a person clears their hep B infection are they contagious/infectious?

If a person has chronic hep B are they infectious?

A

Patients can be infectious for 5 to 15 weeks after onset of symptoms if they clear the infection.

Individuals who develop chronic disease will remain infectious indefinitely.

25
Q

Which hepatitis is most likely to be asymptomatic in the acute phase? Why is this important (2)?

hint: think longterm

A

hepatitis C virus is most often asymptomatic in the acute phase of infection

> 75% of patients advance to the chronic stage..

hepatitis C virus is one of the most common causes of hepatocellular carcinoma

26
Q

How is hep C virus transmitted?

A

mostly blood

27
Q

Acute illness (n/v malaise) with liver enzyme abnormalities could be a few other viruses (not the classic hep ones)… try to name 3

A
  • cytomegalovirus (CMV)
  • herpes simplex virus (HSV)
  • Epstein-Barr virus (EBV)
  • coxsackievirus

Acute illness with liver function test abnormalities can also be caused by infection with other hepatotropic viruses. These agents are unlikely to cause clinically significant hepatitis in an otherwise healthy host.

28
Q

Generally treatment for acute phase hepatitis is supportive.
Which one might you consult for?
What should you keep an eye out for? How?

A

Consult for Hep B - can potentially be treated with antivirals or interferon.

Monitor for signs of progression to fulminant liver failure

  • reassess for worsening signs and symptoms
  • trend lab abnormalities
  • could ask for consult for advice on lab monitoring suite and timeline
29
Q

There are 50 types of these that can cause acute liver toxicity. They are found out in nature. What are they?

A

Mushrooms!

30
Q

What is the most life threatening cause of ascites?

A

SBP is the most common life-threatening complication of ascites

31
Q

Your CHRONIC LIVER FAILURE patient presents to ER with fever and abdo pain, what should you definitely think? How to definitively diagnose this?

A

The classic presentation of SBP is fever and diffuse abdominal pain and tenderness

Paracentesis, send for micro and culture

32
Q

What are three familial disorders that can result in severe chronic disease and liver failure?

A

Wilson’s disease (copper over load)
hemochromatosis (iron overload)
α1-antitrypsin deficiency

33
Q

What element is the issue in Wilson’s disease, what is the serum test you can order?

A

Copper, Ceruloplasmin

Wilson disease is a rare inherited disease that causes too much copper in your blood. Ceruloplasmin is a protein made in your liver. Ceruloplasmin test is used to measure how much of a copper-containing protein is in your blood.

34
Q

Pregnant woman, 30 weeks, present to ER with RUQ pain. Initial labs show low hgb, low platelets, mild transaminitis. What life threatening diagnosis can you not miss?

A

Pregnant women can present with various hepatic or cholestatic disorders not specific to pregnancy.

HELLP syndrome (hemolysis, elevated liver
enzymes, low platelets), however, stands apart as a life-threatening process that must not be missed in the ED. 

HELLP occurs as part of the preeclampsia–eclampsia spectrum in the late third trimester or in the postpartum period.

35
Q

What is the classic history of biliary colic?

hints: location, timing, association

A
  1. EPISODIC RUQ or epigastric pain associated with nausea and vomiting
  2. episodes typically last <6 hours and resolve spontaneously
  3. often in association with fatty meals
36
Q

What are the primary history differences between cholecystitis and cholelithiasis? (2)

A
  1. biliary colic >6 hours

2. constitutional symptoms such as fever and malaise.

37
Q

Ascending cholangitis is described by two classic combinations of findings.
name them and their clinical features

A

charcot’s triad - fever, jaundice, RUQ

reynolds pentad - charcots + hypotension + confusion!!

38
Q

What is a HIDA scan

When to order it - for what ddx and after what other test?

A
  1. a nuc med imaging test of gallbladder FUNCTION (radioactive tracer).
  2. for ?cholecystitis or cystic duct obstruction
  3. indicated if US is equivocal or negative in the presence of a high clinical suspicion (90-94% sensitive for the presence of acute cholecystitis)

Rare in ED b/c HIDA performs more poorly if the patient has eaten within the last 24 hours and that it requires a long period of monitoring after tracer infusion (up to 4 hours).

39
Q

What is MRCP?

Why might you do this before ERCP?

A

Magnetic resonance cholangiopancreatography (MRCP) is a special type of MRI exam that produces detailed images of the hepatobiliary and pancreatic systems, including the liver, gallbladder, bile ducts, pancreas and pancreatic duct.

ERCP is INVASIVE! Endoscopic. Higher risk of complications. Consider doing MRCP first to confirm the need for therapeutic ERCP not just diagnostic ERCP.

40
Q

Treatment of biliary colic

A

Episodes of biliary colic associated with cholelithiasis are typically self-limited and should be treated symptomatically with antiemetics, fluids, and appropriate pain control (NSAIDs and/or opioids).

Definitive tx is cholecystectomy so referral to gen surg and low fat meals until then.

41
Q

Definite treatment of choledocolithiasis?

A

surgical or endoscopic (ERCP) removal of the stone

42
Q

Management of cholecystitis?

A

Symptoms - NPO, IV fluids, pain, nausea
Surgical consult
Abx - ceft/metro or pip-tazo if severe

43
Q

What procedure might be indicated in a critically ill patient with cholecystitis or cholangitis?

A

percutaneous decompression (cholecystostomy) with a biliary drain

44
Q

Most important instructions for someone you discharge with biliary colic who you have referred to gen surg

A

RTER if episode lasts >6 hrs
RTER if fever or jaundice develops

Both would need further and more urgent management