Liver Flashcards

0
Q

How does the liver help maintain blood glucose levels?

A

After a meal, hepatocytes take up glucose and make glycogen (also takes up amino acids and makes proteins) Between meals it breaks down glycogen and releases glucose

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1
Q

___% of bile acids are reabsorbed in the intestine and recirculated

A

90%

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2
Q

How does unconjugated bilirubin become conjugated in order to be excreted?
Hemoglobin -> Heme -> biliverdin -> unconjugated bilirubin (lipid soluble) + _____ + _____ ->conjugated bilirubin excreted with bile

A

Albumin in the plasma and glucuronic acid in the hepatocytes in the liver makes conjugated bilirubin (water soluble)

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3
Q

Is fibrosis reversible in the liver?

A

No, fibrosis is an irreversible consequence of hepatic damage and has lasting consequences on patterns of blood flow and perfusion of hepatocytes

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4
Q

What do elevated ALT and AST mean?

A

A liver cell dies and spills its guts into the blood
Normal is under 50, elevated levels mean the liver cells are dying, liver injury
These are hepatocyte integrity labs

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5
Q

What are elevated alkaline phosphatase and GGT indicative of?

A

These are biliary tract integrity labs
Alk phos is found in the liver and bone. So if it is elevated, look at the GGT, a specific lab to the biliary tract, to see if it is a bone or biliary problem.

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6
Q

How can you determine a level of unconjugated bilirubin using total and direct bilirubin levels?

A

Direct is conjugated. Total is conjugated and unconugated.

Total - direct = unconjugated

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7
Q

If albumin is low, does that mean there is a liver issue?

A

Not necessarily, but if albumin and total protein levels are low, that is a liver problem!

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8
Q

How does prothrombin time relate to the liver? What about ammonia and the liver?

A

The liver makes clotting factors, with liver dysfunction, time will go up before clotting.
Ammonia also goes up with liver dysfunction, it can’t filter the toxins.

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9
Q

With liver disease, will albumin, ammonia, and glycemia levels be hyper or hypo?

A

Hypoalbuminemia
Hyperammonemia
Hypoglycemia (liver can’t break down glycogen and release glucose between meals)

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10
Q

What are other signs of liver disease?

A

Jaundice, cholestasis
Fetor hepaticus (breath of death, liver can’t dump stuff to biliary system, so it excretes in the lungs)
Hypogonadism, gynecomastia (liver can’t get rid of steroid hormones, estrogen raises, FSH/LH fall, less stimulus in gonads)
Palmar erythemia, spider angiomas (estrogen relaxes capillary beds, inc blood flow)
Weight loss, muscle wasting

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11
Q

What are signs of portal hypertension?

A

Ascites, esophageal varices, hemorrhoids, caput medusae, splenomegaly
Inc interstitial pressure causes edema of the GI (ascites)
The three portal systems that blood backs up to are rectum, lower esophagus, and umbilicus

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12
Q

List life-threatening complications of liver disease

A
Multiple organ failure
Coagulopathy
Hepatic encephalopathy
Hepatorenal syndrome
Esophageal varices rupture
Hepatocellular carcinoma
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13
Q

Jaundice (excess bilirubin in the blood): causes?

A
  1. Increased unconjugated bilirubin (lipid soluble, bound to albumin, not excreted): excess bilirubin production, reduced hepatic uptake, impaired conjugation. Note: unbound plasma fraction diffuses into tissue (brain), toxic injury
  2. Increased conjugated bilirubin (water soluble, not bound, excreted by kidney): decreased hepatocellular excretion, impaired bile flow
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14
Q

Cholestasis features of hepatocytes?

A

Hepatocytes are enlarged, contain apoptotic cells, and kupffer cells have bile pigments (regurgitated)
Obstructed portal tracts can cause edema, bile retention, and neutrophilic inflammation
Hepatocytes are swollen and undergoing toxic degeneration

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15
Q

Cirrhosis causes what? Portal hypertension causes what?

A

Cirrhosis impairs blood flow causing portal hypertension
Portal hypertension causes ascites, porto-systemic shunts (esophageal varices, hemorrhoids, caput medusae), and splenomegaly

16
Q

Decreased bile in the GI causes what color stools? What color urine? Why would they be more likely to bleed?

A

Light-colored stools
Dark urine
Decreased vitamin K absorption -> bleeding

17
Q

Hep A and E have what in common? How is it transmitted?

A

They are acute, 2-8 week incubation
Don’t cause carrier state, cancer, or chronic hepatitis
Oral transmission due to poor hygiene, not common in US

18
Q

Which hepatitis can we vaccinate?

A

A and B

If you don’t get hep B, you can’t get hep D

19
Q

Which hepatitis is usually an endemic seen in travelers and has a high mortality rate in pregnant women

A

Hep E

20
Q

Which hepatitis can cause liver cancer?

A

Hep B and C

21
Q

Which hepatitis is more common in children, dangerous in adults, and is usually a sporadic infection associated with oysters

A

Hep A

22
Q

What do Hep B, C, and D have in common? How is it transmitted?

A
Cause carrier state
Cause chronic hepatitis
Cause cancer (D not increased over B)
Parenteral transmission (closer personal contact)
Present in US
23
Q

What is the progression of alcoholic liver disease? What steps are irreversible?

A

Hepatic steatosis (fatty liver)
Alcoholic hepatitis
Cirrhosis - irreversible step

24
Q

What is Hemochromatosis?

A

Uncontrolled uptake of iron (1g/year)
Autosomal recessive disease, more seen in Scotland and Africa
Problems appear later (over 50) and more in men
Problems include cirrhosis, DM, and skin pigmentation
Note: another primary iron overload disease is bantu siderosis

25
Q

List some secondary iron overload diseases

A

Transfusions (1 transfusion has 0.25g iron)

B-thalassemia and sideroblastic anemia (ineffective erythropoiesis)

26
Q

What are some causes of obstructive biliary tract disease (can lead to secondary biliary cirrhosis)

A

Gallstones
Biliary atresia (in children, tract doesn’t open)
Malignancies of biliary tree or pancreas
Strictures from surgery
Note: primary biliary cirrhosis is autoimmune leading to high alk phos and GGT

27
Q

What are some causes of hepatocellular carcinoma? What is the mean survival time?

A
Hep B (especially early Hep B - China)
Chronic liver disease (hep C, alcohol)
Aflatoxin (used to be in peanut butter)
Tyrosinemia
Cirrhosis
Survival is 7 months
28
Q

Cholelithiasis: risk factors for cholesterol stones, risk factors for pigment stones?

A

Cholesterol stones: Fair, Forty, Female, Fertile, Fat, gallbladder stasis, hyperlipidemia
Pigment stones: chronic hemolyic syndrome, biliary infection, GI disorder, Asian
Symptoms: RUQ pain after a fatty meal

29
Q

What is choledocholithiasis?

A

Stones in the biliary tree
Problems include biliary obstruction, pancreatitis, cholangitis, hepatic abscess, chronic liver disease with biliary cirrhosis, acute calculous cholecystitis

30
Q

Causes of pancreatitis?

A

I GET SMASHED (don’t worry about mashed)

Idiopathic, Gallstone, ETOH, Trauma, Steroids