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GI System > Hepatology > Flashcards

Hepatology Flashcards

1
Q

What percentage of cardiac output runs through the liver? What are the sources and proportions of that blood flow?

A

About 25% of cardiac output will go through the liver; the hepatic artery provides 20-40% of flow, the portal vein provides 60-80%

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2
Q

What are the contents of portal vein delivery?

A

Pancreatic hormones, nutrients, drugs, toxins, bacteria, and cells (why the liver is a common site of metastasis)

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3
Q

How are the hepatocytes regionally classified into zones?

A

Hepatocytes near the portal triads are in zone 1; those by the central vein are in zone 3; those in the middle are in zone 2

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4
Q

What are some of the structural distinctions of the sinusoids and how do they affect hepatic blood pressure?

A

Sinusoidal endothelial cells do not adhere to each other very much; their basement membranes are highly fenestrated. These allow rapid diffusion to the hepatocytes and helps to keep hepatic blood pressures low

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5
Q

What happens to the sinusoids with chronic liver damage? What happens to some hepatocytes with chronic liver damage?

A

Stellate cells are activated to deposit matrix components into the space of Disse and the endothelial cells start to interact with each other more readily; some hepatocytes will convert to mesenchymal cells

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6
Q

What is the major consequence of sinusoid capillarization?

A

Resistance of the blood vessels increases and the portal pressures rise (portal hypertension)

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7
Q

What is the definition of cirrhosis?

A

It is a progressive disease caused by diffuse damage to parenchymal cells with nodular regeneration, fibrosis, and architectural disturbances in the liver (nodular regeneration and fibrosis are required for diagnosis)

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8
Q

What are some etiologies of cirrhosis?

A

Hepatitis, chronic alcohol intake (zone 3 damage), fatty liver disease

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9
Q

What chemicals change composition in the portal system as structural alterations in disease happen?

A

Nitric oxide (vasodilator) drops; endothelin (vasoconstrictor) increases

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10
Q

What is the body’s initial response to portal hypertension?

A

The changes in vascular resistance promote splanchnic vasodilation; which actually makes the problem worse by increasing flow to the liver (Pressure=resistance x flow)

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11
Q

What is a major effect of portal hypertension to the vasculature?

A

Excess portal blood tries to escape the portal system via anastomoses near the esophagus, umbilicus, and anus. Varices develop that can hemorrhage

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12
Q

What are cardiac responses to portal hypertension?

A

Increased heart rate and cardiac output, but decreased total peripheral vascular resistance; poorly responsive to vasoconstrictors

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13
Q

What is the kidney’s response to portal hypertension?

A

The kidney senses vasodilation in the splanchnic system as a loss of blood volume and promotes sodium reabsorption to retain additional water. Ascites starts to develop

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14
Q

Why are ALT and AST good lab tests to perform with liver damage?

A

Since the liver is the lone site of amino acid transformation and nitrogen elimination, ALT and AST are almost exclusively in the liver; their presence in the blood is indicative of hepatocytolysis

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15
Q

What is the physiological consequence of excess ammonia from hepatic failure?

A

Hepatic encephalopathy (high ammonia levels cause the brain to shunt ammonia into alpha-ketoglutamate and oxaloacetate; Krebs cycle starts to shut down. Glutamate used to make GABA as well–which is lost)

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16
Q

What classes of serum proteins does the liver produce?

A

1) Proteins that bind and transport hormones and metals
2) Blood coagulants and inhibitors
3) Protease inhibitors

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17
Q

What is the significance of acute phase reactants?

A

In acute stressing situations, the liver will significantly upregulate its production of certain proteins; the hallmark is CRP, which rises with any inflammatory process.

18
Q

What class of enzymes catalyze phase I drug reactions? What three cofactors or substrates are required for them to complete their reactions?

A

Cytochrome P-450 family (CYP); need O2 as a substrate and heme and NADPH as cofactors

19
Q

Where do phase I reactions happen in hepatocytes?

A

Endoplasmic reticulum

20
Q

How do inducers affect drug metabolism in phase I? What effect do inhibitors have?

A

Inducers speed up the cytochrome’s reactions, so it weakens the effect of drugs; inhibitors slow their reactions and enhance drugs

21
Q

What is the goal of phase II drug reactions?

A

Conjugation of a substrate to a polar compound helps to improve a drug’s solubility for excretion

22
Q

How is acetaminophen regularly metabolised by the liver?

A

95% of the ingested compound is metabolized by phase II reactions that add sulfates or glucuronides; residual five percent handled by cytochrome P450s that create a toxic intermediate neutralized by glutathione

23
Q

What happens to the liver with acetaminophen overdose?

A

The phase II pathway exhausts its enzyme supply, so there is a shift to phase I reactions. If the liver’s supply of glutathione is depleted, hepatocyte failure occurs and liver death is a possibility

24
Q

What makes up bile?

A

Bilirubin, bile acids, amino acids, cholesterol, water, and electrolytes

25
Q

How does bilirubin come about?

A

When RBCs die or when cytochromes are recycled, their heme is cleaved to save iron; the porphyrin portion is transformed to bilirubin via biliverdin reductase

26
Q

How does conjugation of bilirubin occur?

A

Hepatocytes use UDP glucuronyl transferase to add glucuronide groups to the carboxyl ends of bilirubin to make it more soluble. Most bilirubin in adults is conjugated twice

27
Q

How is bilirubin secreted?

A

Bilirubin is transported to hepatocytes by albumin and is conjugated there. It then enters the bile canaliculus via the cMOAT transporter (an ATP binding cassette)

28
Q

What are the consequences of elevated unconjugated hyperbilirubinemia?

A

If unconjugated, can cross cell membranes, including the blood brain barrier. When it rises in the brain, the term is kernicterus (unconjugated bilirubin is cytotoxic)

29
Q

What is the genetic cause and consequence of Gilbert’s syndrome?

A

Mutations in the promoter region of UDP glucuronyl transferase reduce the amount of enzyme made; mild elevated hyperbilirubinemia occurs

30
Q

What is the genetic cause and consequence of Crigler-Najar syndrome?

A

Mutations in the coding region of UDP glucuronyl transferase yield a non-functional enzyme and requires a liver transplant to cure.

31
Q

What is the genetic cause and consequence of Dubin-Johnson syndrome?

A

cMOAT mutations inhibit the export of conjugated bilirubin into the bile canaliculus

32
Q

What is the genetic cause and consequence of Rotor syndrome?

A

Mutations in the OATP transporter (to get bilirubin into hepatocytes) yields an elevated conjugated bilirubin level

33
Q

What consequence occurs in patients with OATP mutations?

A

Hepatocytes are unable to metabolize statins well; high statin levels in the blood are myotoxic and rhabdomyelysis can result

34
Q

What are the primary bile acids and what type of cell produces them?

A

Hepatocytes make chenodeoxycholic acid and cholic acid

35
Q

What are the secondary bile acids and what types of cells produce them?

A

Most secondary bile acids are products of bacterial metabolism and include lithocholic acid, ursodeoxycholic acid, and deoxycholic acid

36
Q

How are bile salts added to bile?

A

They are exported using ATP against their concentrations gradient via the BSEP

37
Q

What is the genetic cause and consequence of progressive familial intrahepatic cholestasis?

A

PFIC1 and 3 are mutations in chaperone molecules, so some minor jaundice and intermittent cholestasis occurs; PFIC 2 is more serious as there is a mutation in BSEP and bile salts cannot be excreted–>cirrhosis

38
Q

Where are most bile salts recycled in the intestines?

A

Terminal ileum

39
Q

What is the consequence of high bile acids in the stool?

A

Diarrhea due to water being drawn into stool

40
Q

What are the contributing factors of cholelithiasis?

A

High saturation of cholesterol in bile, low motility, and nucleation of crystals

41
Q

What risk factors contribute to cholesterol stones?

A

Increased age, female sex, Native American ancestry, weight changes, medications, diabetes

42
Q

What are causes of pigmented stones?

A

Calcium bilirubinate from chronic hemolysis, cirrhosis, and chronic infections

GI System (6 decks)

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