Lectures 17, 18: Intro to Liver and LFTs Flashcards

1
Q

Liver functions

A

Excretion (biliubin, bile acids, drugs), immune function, growth factor, hormone production, hematopoiesis (fetal), synthesizes proteins (albumin, clotting factors), substrate metabolism, storage, metabolizes drugs

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2
Q

Signs of liver failure

A

Loss of clotting factors –> coagulopathy; impaired bilirubin clearance –> jaundice; impaired glucose mobilization –> hypoglycemia; impaired metabolite clearance/detox –> encephalopathy; altered blood flow regulation –> renal failure

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3
Q

Signs of liver failure (2)

A

Reduced clearance of bacteria from portal blood –> sepsis; decreased growth factor/albumin –> anemia, edema; altered metabolism of hormones –> feminization; obstruction to blood flow –> portal HTN

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4
Q

The endothelium within the sinusoid of the liver is…

A

Fenestrated

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5
Q

What two specialized cells are in the sinusoid?

A

Hepato-stellate cell encircling the microvasculature and the hepatocyte

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6
Q

Liver macrophage specialized cell

A

Hepatic Kupffer Cell

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7
Q

Bile is secreted through the

A

Canaliculi system

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8
Q

Liver bloods supply and implications; __________ pressure/___________ capacitance

A

Dual: 2/3 through portal vein, 1/3 through hepatic artery; low pO2, easy for areas near central vein to become hypoxic AND liver is RARELY infarcted; low pressure and high capacitance

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9
Q

What drains into the portal vein? (3)

A

Splenic, coronary, mesenteric

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10
Q

Examples of acute injury and significance for transplant

A

Tylenol, viral infection, idiopathic; may require transplant if severe, but if it resolves, liver will return to normal

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11
Q

Examples of chronic liver injury and significance for transplant

A

Viral infection, alcohol, obesity-related, autoimmune, metabolic overload, biliary obstruction; chronic liver injury is progressive and may be asymptomatic

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12
Q

Histology of cirrhosis

A

Nodules surrounded by fibrous tissue

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13
Q

Complications of cirrhosis (5)

A

Hepatic encephalopathy, ascities, portal HTN, hepatorenal syndrome, splenomegaly

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14
Q

What tests reveal injury to hepatocytes?

A

AST, ALT bili

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15
Q

What tests reveal injury to bile ducts?

A

Alkaline phosphatase, gammaGT, bili

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16
Q

Four classes of dx liver tests

A

Liver enzymes, liver function tests, general systemic tests, liver imaging

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17
Q

Liver enzymes tested

A

AST, ALT, Alk Phos, Bili

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18
Q

Liver function tests

A

Albumin, prothrombin time, platelets

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19
Q

General systemic tests

A

CBC, renal fxn tests (BUN/creatinine)

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20
Q

Signs of chronic liver disease (9)

A

Scleral icterus, spider angioma, glossitis, palmar erythema, digital clubbing, gynecomastia, excoriations (marks from itching), xanthelasma, ascites

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21
Q

What’s the most common cause of spider angiomata?

A

Pregnancy due to estrogen

22
Q

Bilirubin must be greater than this level to cause jaundice…causes

A

2.5 mg/dL; increased bilirubin production, impaired hepatic handling, or benign

23
Q

Two sources of bilirubin and %

A

Erythrocytes (80%); non-hemoglobin hemoproteins (myoglobin, cytochromes, catalases; 20%)

24
Q

Describe bilirubin in plasma

A

Unconjugated (insoluble), albumin-bound, total bilirubin = 1-1.5 mg/dL

25
Q

Four steps of bilirubin (blood to bile)

A
  1. Hepatocellular uptake; 2. Intracellular binding; 3. Conjugation; 4. Excretion into bile canaliculus via MRP2 (multidrug resistance-associated protein 2)
26
Q

Does bilirubin enter the hepatocyte alone or with albumin?

A

Alone

27
Q

Enzymes of bilirubin conjugation

A

UGT = bilirubin-UDP-glucuronosyltransferase

28
Q

Injury to the hepatocyte tends to affect with step of the bilirubin?

A

Liver can conjugate but NOT EXCRETE bilirubin (MRP2 is impaired) –> CONJUGATED bilirubin backs up into sinusoid –> central venule –> systemic circulation

29
Q

Why is stool/urine the color it is?

A

Yellow urobilinogen (gets turned into brown stercobilin in colon)

30
Q

Bilirubin + intestine

A

In ileum/colon, unconjugated and reduced to urobilinogen –> 80% feces, 15% absorbed and re-excreted as bile, 5% excreted in urine

31
Q

Bilirubin + kidney

A

Conjugated bilirubin is filtered at glomerulus; with hepatobiliary dysfunction, conjugated bilirubin gets into kidneys –> darker urine

32
Q

Causes of unconjugated hyperbilirubinemia (3)

A
  1. Increased production of bilirubin, 2. Reduced hepatic clearance of bilirubin, 3. Inherited disorders
33
Q

Causes of increased production of bilirubin

A

Hemolysis, hematomas, ineffective erthropoiesis

34
Q

Causes of reduced hepatic clearance of bilirubin

A

Neonatal jaundice (due to hepatic immaturity, tx w/ phototherapy), breast milk jaundice (maternal progestational steroids inhibit conjugation), drugs (antibiotics)

35
Q

Inherited disorders of bilirubin conjugation (3)

A

Gilbert’s syndrome, Crigler-Najjar type I and type II

36
Q

Describe Gilbert’s syndrome: frequency and %, symptoms, histology, gene, and enzyme activity

A

Most common hereditary hyperbilirubinemias (7%), asymptomatic but aggrevated by stress, no histological changes, UGT1A1 gene mutation, 10-33% of normal enzyme activity

37
Q

Describe Crigler-Najjar Syndrome type I: mutation, enzyme activity, when it presents and complication, tx

A

Mutation in UGT1, no functional enzyme activity, appears neonataly, severe neurological impairment, fatal w/out transplant

38
Q

Describe Crigler-Najjar Syndrome type II: mutation, enzyme activity, tx

A

Mutation of UGT1A1, reduced but detectable enzyme activity, tx = phenobarbital to induce UGT

39
Q

Conjugated hyperbilirubinemia diseases (5 classes)

A

Genetic, chronic liver disease (cirrhosis), biliary obstruction, intrahepatic cholestasis of pregnancy, drug-induced cholestasis

40
Q

Genetic causes of conjugated hyperbilirubinemia diseases (3)

A
  1. Dubin-Johnson syndrome, 2. Rotor syndrome, 3. Familial Cholestasis syndromes
41
Q

Describe Dubin-Johnson syndrome: mutation and presentation

A

Mutation in MRP2 with chronic intermittent jaundice and pigmented liver, scleral icterus, enlarged liver

42
Q

Describe Rotor syndrome

A

High total bilirubin with normal life expectancy (unknown mutation, not much known)

43
Q

Causes of biliary obstruction

A

Choledocholithaisis, neoplasms, extrinsic compression of biliary tree, inflammation/infection

44
Q

Describe intrahepatic cholestasis of pregnancy: when in pregnancy, lab tests, does it go away?

A

2nd/3rd trimester, elevated ALT, bilirubin, bile acids; generally disappears after delivery but may reappear with other preg/estrogens

45
Q

Three most common scenarios of acute hepatocellular inury and LFTs

A

Ischemic injury (“shock liver” = trauma), drug-induced liver failure, acute viral hepatitis; elevated ALT, AST, some bilirubin, all else likely normal

46
Q

Five most common scenarios of chronic liver disease/cholestatic liver disease

A

Chronic viral hepatitis, NAFLD, alcoholic hepatitis, cirrhosis, biliary obstruction

47
Q

Cirrhosis: LFTs

A

ALT, AST, Alk Phos, GGTP, Bilirubin NORMAL or slightly elevated; elevated prothrombin time, low albumin

48
Q

Biliary obstruction: LFTs

A

ELEVATED Alk Phos, GGTP, bilirubin; normal or slightly elevated ALT, AST, fxn tests

49
Q

Chronic viral hepatitis and NAFLD: LFTs

A

Elevated ALT, AST, normal or slightly elevated cholestasis, normal fxn tests

50
Q

Alcoholic hepatits: LFTs

A

Elevated AST > ALT (specific to alcoholic), elevated cholestasis, normal fxn tests