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Clin Med 2 > Acute and Chronic Liver Disease Lectures > Flashcards

Acute and Chronic Liver Disease Lectures Flashcards

1
Q

Where does the majority of blood in the liver come from?

A

port vein –from intestines (60%)

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2
Q

What is the portal triad?

A

hepatic artery
portal vein
bile duct

entering into the liver

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3
Q

Kupffer cell

A

a macrophage in the portal space that works to remove endotoxins to prevent it from going into the systemic circulation

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4
Q

Stellate cells

A

within the space of disse (space between sinusoid and hepatocytes)

normally these cells are benign –simply storing vitamin A

however when they get activated or damaged they form COLLAGEN

in between the endothelial lining and the hepatocytes —this is where these cells are and where scaring occurs

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5
Q

What are the functions of the liver?

A

detox
synthesizes plasma proteins —clotting factors
synthesize lipids, lipoproteins, glucose
synthesize and metabolize endocrine hormones
Ag-Ab complex removal (Kupffer cells)

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6
Q

LFTs

A

hepatic panel

  • bilirubin - total and direct
  • AST - asparate aminotransferase
  • ALT - alanine aminotransferase
  • AlkP or AP (alkaline phosphatase)
  • Albumin

the real “function” tests of the liver are bilirubin, albumin, and PT

the others are only measures of enzymes released from injured cells

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7
Q

How is bilirubin carried to the liver?

A

by albumin

carries UGB to the liver to become CB

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8
Q

How does the liver metabolize bilirubin?

A

conjugate it to diglucuronide with UDPG

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9
Q

What happens to diglucuronide?

A

it gets stored in the bile where it slowly gets sent into the intestine where bacteria break it down further into urobilinogen and sterobolinogen (which makes your stool brown)

urobilinogen has two fates —one is to be converted to sterobolinogen which becomes feces
the other is to get absorbed into the blood where it becomes urobilin which gets filtered in the kidney and makes urine yellow

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10
Q

Direct vs indirect bilirubin?

A

direct is conjugated bilirubin (water soluble) –most commonly diglucuronide

indirect is unconjugated (not water- soluble) –only form in normal plasma –increase by hemolysis —always bound to albumin

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11
Q

When you see an increased indirect bilirubin, what does that mean?

A

higher unconjugated bilirubin
always bound to albumin

increased d/t hemolysis

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12
Q

If you see a decrease in albumin what does this mean?

A

This decrease has to be d/t a chronic liver disease because it takes 20 days before you will see a decrease in albumin d/t its half life of 20 days

remember that the liver is the ONLY source of albumin

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13
Q

What does a prolonged PT in a normal pt mean?

A

The liver is not making the necessary clotting factors

the first thing you want to try is give vitamin K —it the PT corrects then the problem is probably not in the liver but in the absorption of vitamin K

you need vitamin K for clotting factors to work

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14
Q

Which tests on the liver panel tell you about cell injury/inflammation?

A

AST

ALT

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15
Q

Which test is more liver specific, AST or ALT?

A

ALT

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16
Q

What does elevated AST mean?

A

it could mean many things because it is found in high concentrations in the heart, kidney, muscle, and liver

so it could be elevated due to running a marathon, etc.

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17
Q

In most cases of liver injury, what do you expect to see with AST and ALT?

A

ALT > AST

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18
Q

What if you see AST > ALT?

A

could be:

  • sudden acute liver necrosis
  • EtOH-related liver injury
  • cirrhosis and/or malnutrition
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19
Q

What does a rise in AlkP mean?

A

a possible obstruction in the biliary tree or the parenchyma of the liver

this is because alkaline phosphatase is release from the cell membrane of hepatocytes in the canalicular membrane when bile is blocked up and resting on the membrane too long

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20
Q

What tests are used to detect cholestasis?

A

bilirubin
AlkP
GGT

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21
Q

At what level will you start to see jaundice?

A

when the bilirubin is 2X the normal level

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22
Q

If you have a higher indirect bilirubin compared to direct bilirubin, what might this mean?

A

That the problem is with hemolysis

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23
Q

What sxs might you see in chronic cholestasis?

A

The bile can’t get out so it accumulates in the blood (pruritic rash) and in the skin (xanthelasma and xanthomata)

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24
Q

Pts with steatorrhea might have deficiency in vitamin A, D, E and K, why?

A

because if they aren’t able to absorb fats they aren’t absorbing fat-soluble vitamins

remember with the prolonged PT you should first try and see if the pt responds to vitamin K

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25
Q

What sxs might you see in chronic liver disease?

A 
palmar erythema 
clubbing
spider angiomata (blanching) 
gynecomastia 
testicular atrophy
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26
Q

Why do we want to keep the pressure down in pts with cirrhosis?

A

put them on prophylaxis BB (propranolol) to try and precent the formation of varices

27
Q

What annual screening should be done with cirrhosis pts?

A

do endoscopy looking for esophageal varices (and treat if they have them)

these are under such high pressure that if they rupture they will bleed like an artery and have a 40% chance of killing the pt

28
Q

What is the management of ascites?

A 
d/c NSAIDs
avoid renal toxic drugs (aminoglycosides) 
2g sodium diet 
do not restrict water 
spironolactone or furosemide

monitor treatment with daily weights (goal weight loss 1-2 lb/day)

29
Q

Refractory ascites

A

ascites that doesn’t respond to our treatment

poor prognosis

30
Q

What is the treatment for hepatic encephalopathy?

A

restrict dietary protein in diet
lactulose (nonabsorbable sugar)
Rifaxamin or neomycin (nonabsorbale ABX)

31
Q

Lactulose

A

non-absorbable sugar used in hepatic enchpalopathy

maintains regular bowel movements
favors growth of lactobacilli in gut that compete with more amminogenic bacteria and tend to produce a more acidic environment
may contribute to acidification of gut

32
Q

Hepatorenal syndrome

A

NOT DONE HERE

33
Q

What is primary biliary cirrhosis?

A

PBC

idiopathic autoimmune of INTRAhepatic small bile ducts thus decrease bile salt excretion

34
Q

Who gets PBC?

A

middle aged (40-60) age WOMEN

35
Q

I GET SMASHED

A

causes of acute pancreatitis:

I- idiopathic
G- gallstones
E- EtOH
T - trauma 
S - steroids
M - mumps virus 
A - autoimmune dz
S - scorpion sting 
H - hyperTG + hypercalcemia
E - ERCP 
D - drugs
36
Q

What is the difference between zone 1 and zone 3 of the liver?

A

Based on oxygenation
Zone 1 - around the portal veins –most oxygenated blood
Zone 3 - around the central vein –least oxygenated blood

37
Q

Where is albumin made?

A

liver

liver is the ONLY source of albumin

38
Q

What is happening to bilirubin in the liver?

A

after UCB (indirect) has been transferred to the liver via albumin, it is digested via UDPG or UGT to form direct bilirubin aka diglucuronide

this will then get stored in the bile where it eventually will be released into the gut and broken down by bacteria into urobilinogen (reabsorbed into blood and excreted in urine) and then broken down into stercobilin which gets excreted in poop

39
Q

Will you see higher conjugated or unconjugated bilirubin in cholestasis?

A

higher conjugated bilirubin

the liver is still turning UCB to CB
the gallbladder is just having a build up of CB

40
Q

Will you see higher conjugated or unconjugated bilirubin in hepatitis?

A

higher UCB

problem at the site of the liver

the UCB is getting to the liver just not getting formed into CB

41
Q

What are major causes of jaundice in adults?

A

Prehepatic - inherited disorders like Gilberts

Hepatic - cirrhosis
hepatitis

Biliary tree - obstruction

42
Q

What is the initial test of choice for bile duct obstruction like cholestasis?

A

US

43
Q

What is the difference between collagen types in a normal liver vs a cirrhotic liver?

A

Normal liver is mainly collagen type 3

Cirrhotic liver is mainly collagen type 1 (best seen with reticulin stain)

44
Q

Why do some pts experience a pruritic rash with cholestasis?

A

more commonly in chronic cholestasis

this is because bile acid cant get out and accumulates in the blood

45
Q

What might steatorrhea tell you?

A

that the pt is not digesting or absorbing fats

this can be caused by decrease cholesterol since cholesterol is needed to make bile acids and bile acids are needed to break down fat

46
Q

Prehepatic causes of portal HTN

A

portal vein thrombosis

47
Q

Hepatic causes of portal HTN

A

Sinusoidal -cirrhosis

48
Q

Posthepatic causes of portal HTN

A

outflow obstruction like cor pulmonale

49
Q

What is normal HVWP?

A

Hepatic venous wedge pressure
HVWP - IVC = < 4mmHg

cirrhosis >4mmHg
really bad if its >12mmHg

50
Q

What is a major and potentially life threatening complication of portal HTN?

A

esophageal varices

under such high pressure that if they rupture they could bleed out

GO TO THE ER if you see blood in your vomit or if you cough blood

51
Q

How can you prophylactically treat pts with risk of esophageal varices?

A

BB - propranolol

52
Q

How do you treat a bleeding esophageal varices?

A

variceal band ligation (standard of care)

53
Q

What heme problems might a pt with cirrhosis have?

A

Splenomegaly (d/t portal HTN)
thrombocytopenia as a result of splenomegaly
impaired synthesis of clotting factors d/t liver fibrosis
assess PT –prolonged indicates a large portion of the liver is not functioning (in the absence of vit K deficiency)

tx: vit K, FFP or platelets, as indicated

54
Q

How do you manage ascites?

A

d/c meds that adversely effect the kidney such as NSAIDS (decrease PG with decrease renal circulation which leads to N+ retention)
avoid renal toxic drugs (aminoglycosides)

2g Na diet
do not restrict water unless hyponatremia

spironolactone
furosemide

daily weights –goal: lose 1-2 lb per day
urine sodium levels

55
Q

What must you do for a pt with new-onset ascites?

A

get a sample of the fluid via tapping to confirm transudate and r/o bacterial peritonitis

56
Q

SBP

A

spontaneous bacterial peritonitis

frequent complication of ascites –occurs in 20% of cases

dx: low grade fever, abdominal tenderness, increase WBC, decrease in pH
increase BUN/Cr
encephalopathy

57
Q

What suggests infection of SBP?

A

peritoneal tap WBC >500
culture at beside of peritoneal fluid
positive urine dipstick for leukocyte esterase

58
Q

What is the treatment for SBP?

A

IV broad spectrum ABX

+/- albumin infusion

PO ABX for at risk pts (rifaxamin or norfloxacin)

59
Q

What are common pathogens causing SBP?

A

E. coli
K. pn
S. pn

60
Q

What are signs of hepatic encephalopathy? What might you see on EEG?

A

triphasic slow waves on EEG

asterixis
mental confusion
constructional apraxia
fetor (odor of mercaptans)

61
Q

How do you treat hepatic encephalopathy?

A

Underlying condition

Consider restricting dietary PROTEIN (protein broken down by bacteria in gut can release NH3)

lactulose - a nonabsorbable sugar –maintains regular bowel movement

consider a non-absorbable ABX -rifaxamin or neomycin

avoid sedation

62
Q

OLT

A

orthoptic liver transplantation

survival after OLT >80% at 5 years

63
Q

What are the indications of OLT?

A

evidence of end-stage liver disease
expected survival < 1 year
clinical decompensation of liver disease

64
Q

What are contraindications of OLT?

A

systemic infections of AIDS (HIV alone is not an absolute contraindication)
Severe cardiopulmonary disease
Metastatic malignancy

Clin Med 2 (13 decks)

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