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Test 4 MCM Leesy > B2.069 - Big Case Liver Failure > Flashcards

B2.069 - Big Case Liver Failure Flashcards

1
Q

What is jaundice clinically

A

Yellow discoloration of skin and mucosal when bilirubin exceeds 2.5 mg/dL

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2
Q

What causes jaundice

A

When the equilibrium between production of bilirubin and the metabolism and excretion is disturbed.

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3
Q

How is bilirubin made in the body

A

Senescent erythrocytes are broken down to heme which is converted to biliverdin by heme oxygenate and biliverdin reductase by mononuclear phagocytic cells

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4
Q

Why cant bilirubin be excreted through the urine

A

Its water insoluble

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5
Q

How is bilirubin excreted from the body

A

Bilirubin is complexed with albumin (major carrier protein in the body) and carries it to the liver for further processing. It then is taken up by the liver cell to be processed. Once inside the hepatocyte its conjugated by UGT1A1. Then it becomes water soluble so it can be secreted by urine or feces. Its secreted from the hepatocyte to the canulicular membrane to the biliary tree then to the gut.

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6
Q

what population is at increased risk of jaundice

A

Premature babies and babies being breastfed

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7
Q

What is Crigler-Najjar syndrome

A

When you have no UGT1A1 which is needed to conjugate bilirubin albumin complex

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8
Q

What is Gilbert syndrome

A

When you have 30% of the UGT1A1 enzyme needed and it causes jaundice during stress

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9
Q

What is the final step of heme breakdown

A

The hepatic ducts join and deposit conjugated bilirubin into the ampulla Vauter

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10
Q

What’s the difference between conjugated and non conjugated bilirubin

A

Conjugated is water soluble and can be excreted

Unconjugated is not water soluble and cant be excreted regardless of how high the blood levels are

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11
Q

What constitutes unconjugated hyperbilirubinemia

A

ratio of conjugated bilirubin:Total bilirubin

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12
Q

What constitutes conjugated hyperbilirubinemia

A

Ratio of conjugated bilirubin:Total bilirubin is >.4

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13
Q

What are causes of overwhelming the first step of heme breakdown

A

Hemolytic anemia
Resorption from internal hemorrhage
Ineffective erythropoiesis

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14
Q

What are causes of impaired canalicular transport of bilirubin

A

Rotor syndrome
Dubin-Johnson syndrome
Drugs

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15
Q

What is physiologic jaundice of newborn due to

A

decreased UGT1A1 activity

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16
Q

What are the two types of Criglar Najjar syndrome

A

Type I - Absense of UGT1A1 this is incompatible with life

Type II - Decreased presence of UGT1A1

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17
Q

What are other diseases of the liver that can cause jaundice

A

Hepatitis, hepatocyte, necrosis, cirrhosis

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18
Q

What are the normal ranges of AST and ALT

A

AST - 7-40

ALT - 7-56

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19
Q

What do AST and ALT do

A

Live in hepatocyte and they are enzymes that help break things down.

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20
Q

What causes raised AST or ALT levels (generally)

A

Anything that compromises membrane integrity of the hepatocyte

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21
Q

What is confluent necrosis

A

Huge zones of hepatocyte necrosis

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22
Q

What happens to the AST and ALT levels of a patient with massive necrosis

A

It will get really high and then fall off because all the hepatocytes are dead

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23
Q

What is secreted in bile

A

Serum bilirubin total and direct

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24
Q

What are the plasma membrane proteins of bile ducts

A

Serum alkaline phosphatase

Serum gamma glutamyl transpeptidase (GGT)

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25
Q

What is the portal triad

A

Artery, vein, bile duct

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26
Q

What does the bile duct look like on histo

A

A string of pearls

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27
Q

What happens when bile ducts are damaged

A

They leak alkaline phosphatase, GGT

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28
Q

What are the lab studies of acute liver disease

A

Increase AST and ALT

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29
Q

What are the lab studies of acute liver failure

A

Increased AST, ALT, prolonged PT, increased ammonia

30
Q

What are the labs of obstructive/biliary liver disease pattern

A

Increased alkaline phosphate, bilirubin and increased GGTP

31
Q

What are the labs for cirrhosis pattern

A

Decreased albumin, decreased platelets, prolonged PT

32
Q

Why do you seen decreased platelets in patients with cirrhosis?

A

Portal hypertension and splenomegaly

33
Q

What does the PT measure

A

extrinsic coagulation pathway

V, VII, IX, X

34
Q

What is hepatic encephalopathy due to

A

Increased in serum ammonia made as a byproduct of hepatocyte processing of nitrogen containing compounds.

35
Q

What does high levels of serum ammonia cause

A

Its toxic to neurons so it causes encephalopathy

36
Q

What are clinical manifestations of increased ammonia

A

Alterations in mental status
Disordered sleep
Asterixis (flapping tremor)
Coma and death

37
Q

What constitutes hepatic failure

A

80-90% of hepatic functional capacity is gone

38
Q

What is the mortality of hepatic failure

A

70-95% without transplant

39
Q

What causes hepatic failure

A

Sudden or massive destruction

End point of progressive damage to liver as part of chronic liver disease

40
Q

What is cirrhosis

A

Scarring of the liver

41
Q

What are symptoms of cirrhosis

A

Decrease of protein synthesis
Portal hypertension
Decreased detoxification

42
Q

What is hyperesterinemia

A

When the liver cant break down estrogen

It causes gynecomastia in men and testicular atrophy

43
Q

What is cirrhosis most commonly caused by

A

Viral hepatitis (50% of HCV develops cirrhosis)
Alcoholic liver disease
NAFLD/NASH

44
Q

What’s the pathogenesis of cirrhosis

A

Progressive fibrosis and reorganization of vascular micro architecture of the liver
Types I and III collagen are deposited in the lobule

45
Q

What does the dying hepatocyte activate

A

Kupffer cells which secrete cytokines and activate stellate cells to become myofibroblasts (secrete mostly type I collage) which is an irreversible process

46
Q

What causes splenomegaly

A

Portal systemic shunts
Blood backs up from liver bc its hard and fibrous which goes into the spleen and causes it to enlarge which sequesters platelets

47
Q

Why do patients with cirrhosis have low platelets

A

Because the spleen is enlarged with blood and it sequesters platelets

48
Q

What is periumbilical caput Medusa

A

When collaterals in the abdominal wall become engorged caused by chronic liver disease

49
Q

What’s a normal reference range for Tylenol

A

Less than 20

50
Q

What are located in the points of each hexagon in the liver lobule

A

Portal tracts

51
Q

What zone does the blood come to in the liver

A

Zone 1

52
Q

Rank the zones of the liver in order of most oxygen to least

A

1>2>3

53
Q

What zone has the most cytochrome p450?

A

Zone 3

54
Q

What does cytochrome p450 do with respect to this big case

A

it breaks down acetometaphen

55
Q

What is the first thing you think of when you thing of centrilobular (zone 3) necrosis

A

Tylenol poisoning

56
Q

Acetometaphen is converted to what toxic enzyme

A

NAPQI

57
Q

How is NAPQI taken care of in the body normally

A

GSH binds with it

58
Q

What is one way to treat acetaminophen overdose?

A

Giving NAC which is converted to GSH which combines with NAPQI to make a non toxic conjugate

59
Q

After the hepatocyte dies can you give NAC

A

No it wont work, most effective in first 12 hours

60
Q

What are the types of drugs that cause liver injury

A 
Antibiotics
Minocycline is big, its for acne
Isoniazid - for TB
Phsychotropic meds
Birth Control pills
61
Q

What is are drugs that cause a cholestatic acute injury

A

Cause canalicular plugs

Caused by anabolic or contraceptive steroid use

62
Q

Alcoholic induced liver disease causes what

A

Steatosis which is fat deposition in the liver

63
Q

What causes steatosis in the liver with alcoholism

A

Production of excess reducing equivalents (NADH and H+) due to metabolism of alcohol

64
Q

How does excess reducing equivalents derived from alcohol metabolism cause steatosis

A

Shunting of normal substrates away from catabolism and toward lipid biosynthesis

65
Q

How many deaths related to cirrhosis are due to alcohol

A

40%

66
Q

Steps of alcohol induced liver disease

A

Steatosis
Steatohepatitis - inflammation of the liver cell
Cirrhosis

67
Q

What is the irreversible point in liver disease

A

Cirrhosis

68
Q

Where is steatosis initially seen

A

Centrilobular

69
Q

Histologically what does inflammation and steatosis of the liver look like in alcoholism

A

Ballooned hepatocytes
Fat droplets large and small
Intermediate filaments called Mallory hyaline

70
Q

What is non alcoholic fatty liver disease due to

A

Obesity
Dyslipidemia
Hyperinsulinemia
Insulin resistance

71
Q

What constitutes Metabolic syndrome

A 
One of these
DM
Impaired glucose tolerance
Impaired fasting tolerance
Insulin resistance
Two of
High blood pressure
Dyslipidemia
Central obesity
Microalbuminuria
72
Q

Steps of NAFLD

A

Steatosis, steatohepatitis, fibrosis

Test 4 MCM Leesy (6 decks)

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