pathology 7 - Cirrhosis and portal hypertension-Serum markers of liver and pancreas pathology-Reye syndrome-Alcoholic liver disease-Non-alcoholic fatty liver disease Hepatic encephalopathy Flashcards

1
Q

During an autopsy, a 52-year-old man from the United States is found to have a shrunken, nodular liver. What is the most likely etiology?

A

Alcohol (responsible for 60–70% of cirrhosis in the United States)

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2
Q

Esophageal varices and caput medusae are caused by ____ (pathologic state) and are partially alleviated by ____ shunts.

A

Portal hypertension; portosystemic

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3
Q

A patient with musty-smelling breath presents to the ED with confusion and asterixis. What skin findings do you expect on exam?

A

Common skin findings in liver failure are jaundice and spider nevi (the musty breath is fetor hepaticus) & may see caput medusae, edema

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4
Q

A patient with melena is found to have esophageal varices. Where else in the GI tract are you concerned for bleeding?

A

The stomach, due to bleeding peptic ulcers (or may be caused by portal hypertension)

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5
Q

Name at least three direct effects of portal hypertension.

A

Splenomegaly, caput medusae, ascites, esophageal varices with hematemesis, peptic ulcers, anorectal varices, portal hypertensive gastropathy

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6
Q

An alcoholic has cirrhosis due to liver failure. What do you expect to find on eye exam?

A

Scleral icterus

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7
Q

While seeing a patient with known cirrhosis, you cannot help but notice his musty breath. What is this called?

A

Fetor hepaticus

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8
Q

Visible dilated capillary proliferation within the skin secondary to the effects of liver failure and cirrhosis is called what?

A

Spider nevi

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9
Q

A man with liver failure also complains of gynecomastia and testicular atrophy. How did this likely develop?

A

Due to an increase in estrogen

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10
Q

A patient with cirrhosis has a coarse, flapping tremor of the hands. What is this called?

A

Asterixis

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11
Q

A cirrhotic patient should be cautioned about what kind of hematologic abnormality(ies) due to her liver cell failure?

A

Bleeding tendency (decreased production of clotting factors, increased prothrombin time) and anemia

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12
Q

Why do patients with cirrhosis have an increased tendency to bleed?

A

Liver cell failure decreases production of prothrombin and clotting factors

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13
Q

Is the bleeding tendency in cirrhosis considered an effect of portal hypertension or an effect of liver cell failure?

A

Liver cell failure (it is due to the inability to synthesize clotting factors)

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14
Q

Is the ankle edema of cirrhosis considered an effect of portal hypertension or an effect of liver cell failure?

A

Liver cell failure (it is due to the inability to synthesize albumin resulting in lack of oncotic pressure)

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15
Q

What is cirrhosis?

A

Cirrhosis is defined as diffuse fibrotic and nodular regeneration that disrupts the normal architecture of the liver

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16
Q

What two gastrointestinal enzymes are markers of injury to hepatocytes?

A

The aminotransferases, which are alanine aminotransferase and aspartate aminotransferase

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17
Q

A patient has viral hepatitis. What do you expect the ratio of aspartate aminotransferase to alanine aminotransferase to be?

A

Low (in viral hepatitis, AST

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18
Q

A patient has alcoholic hepatitis. What do you expect the ratio of aspartate aminotransferase (AST) to alanine aminotransferase (ALT) to be?

A

High (in alcoholic hepatitis, AST > ALT)

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19
Q

A 40-year-old man is intoxicated and not making any sense. Elevated serum γ-glutamyl transpeptidase may indicate which diagnosis?

A

Chronic alcoholism, along with possible Wernicke encephalopathy

20
Q

A patient has elevated alkaline phosphatase. To differentiate between bone disease and liver pathology, what marker do you use?

A

γ-glutamyl transpeptidase (like ALP, GGT is elevated in liver and biliary disease, but unlike ALP, it is not elevated in bone disease)

21
Q

Alkaline phosphatase, in addition to being a marker of liver disease, is also a marker of ____ disease.

A

Bone

22
Q

Which two gastrointestinal enzymes are used as markers for acute pancreatitis? Which one is more specific?

A

Amylase and lipase; lipase is more specific

23
Q

A patient has epigastric abdominal pain radiating to the back, fever, and nausea. What two enzymes will likely be elevated on lab studies?

A

Amylase and lipase will likely be elevated (the patient has acute pancreatitis)

24
Q

Which serum protein is decreased in Wilson disease?

A

Ceruloplasmin

25
Q

A patient has bronze rings in the irises, liver cirrhosis, muscle rigidity, and dystonia. What serum protein is most useful to check?

A

Ceruloplasmin is decreased, because this patient likely has Wilson disease (the bronze rings are Kayser-Fleischer rings)

26
Q

A boy who has never received any vaccines comes to the ED with an elevated amylase level (lipase is normal). Name a likely diagnosis.

A

Mumps

27
Q

A 5-year-old boy with seasonal flu is given aspirin for his fever and develops altered mental status and elevated LFTs. Diagnosis?

A

Reye syndrome

28
Q

What pathologic liver change is associated with Reye syndrome?

A

Microvesicular fatty changes and, later on, hepatomegaly

29
Q

A 7-year-old girl is thought to have Reye syndrome. What metabolic disturbance do you check for (it shows up on a basic metabolic panel)?

A

Hypoglycemia

30
Q

A mother brings in her son for lethargy and vomiting. A week ago he had a viral infection treated with a drug. What was he likely given?

A

Aspirin or salicylates (the boy likely developed Reye syndrome, which can occur in children with viral infections treated with aspirin)

31
Q

A mother asks if she can give her 4-year-old son aspirin for his fever of 101°F. What drug would you recommend instead?

A

Acetaminophen or ibuprofen

32
Q

How does aspirin cause Reye syndrome in young infants?

A

Aspirin metabolites reversibly inhibit mitochondrial enzymes and cause a decrease in β-oxidation

33
Q

There is one fever syndrome for which children are actually encouraged to take aspirin. What is it? Why?

A

Kawasaki disease; aspirin is needed to treat inflammation and prevent clots from forming

34
Q

What potentially reversible liver pathology can be seen with moderate alcohol intake?

A

Macrovesicular fatty changes of the liver (hepatic steatosis)

35
Q

A patient with chronic alcoholism develops hepatitis. What microscopic changes do you expect to see on liver biopsy?

A

Swollen and necrotic hepatocytes with neutrophilic infiltration and Mallory bodies (he likely has alcoholic hepatitis)

36
Q

You test the AST and ALT levels of a long-term alcoholic with sustained alcohol consumption. What do you expect them to be?

A

AST > ALT (the ratio is usually >1.5) (make a toast with alcohol)

37
Q

A 48-y/o woman with chronic alcoholism crashes her car and lacerates her liver. She goes to the OR. How do you expect her liver to appear?

A

She will likely have a micronodular, irregularly shrunken liver (also called hobnail appearance) (this is alcoholic cirrhosis)

38
Q

An alcoholic patient has jaundice, a “hobnail” liver, and hypoalbuminemia. If the patient quits drinking, will these symptoms go away?

A

No, as this describes a micronodular, shrunken liver appearance indicating alcoholic cirrhosis, which is irreversible

39
Q

What is the AST:ALT ratio in non-alcoholic fatty liver disease?

A

ALT > AST (ALT = Lipids)

40
Q

A non-alcoholic, type II diabetic patient has cirrhosis and a high ALT:AST ratio. What pathologic changes are associated with this disease?

A

Insulin resistance = fatty infiltration of hepatocytes & cellular ballooning on pathology (as seen in non-alcoholic fatty liver disease)

41
Q

What type of syndrome is associated with non-alcoholic fatty liver disease?

A

Metabolic syndrome (insulin resistance)

42
Q

A non-alcoholic man with a high ALT:AST ratio and metabolic syndrome should be advised that he is at risk for what type(s) of liver disease?

A

Cirrhosis and HCC (he has non-alcoholic fatty liver disease)

43
Q

A non-alcoholic patient with portosystemic shunt has asterixis. He has eaten only protein powder for the past month. How do you treat him?

A

Treat with lactulose and rifaximin (he is suffering from hepatic encephalopathy), & he should eat less protein (decreases NH3 production)

44
Q

A patient with decreased NH3 metabolism and neuropsychiatric dysfunction presents with profound delirium. How do you treat him?

A

Treat with lactulose and rifaximin (he is suffering from hepatic encephalopathy)

45
Q

What are some triggers of hepatic encephalopathy?

A

Increased NH3 production (protein intake, GI bleeding, constipation, infection), decreased NH3 removal (renal failure, diuretics, TIPS)

46
Q

A patient with hepatic encephalopathy is prescribed lactulose. He is also a medical student who wonders what lactulose does. You say?

A

Lactulose increases NH4+ generation, which decreases NH3 that can contribute to hepatic encephalopathy

47
Q

A patient with hepatic encephalopathy is prescribed a drug that kills intestinal bacteria to prevent NH3 build-up. What is it?

A

Rifaximin