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

Acute and Chronic Liver Disease Lectures Flashcards

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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
What sxs might you see in chronic liver disease?
``` palmar erythema clubbing spider angiomata (blanching) gynecomastia testicular atrophy ```
26
Why do we want to keep the pressure down in pts with cirrhosis?
put them on prophylaxis BB (propranolol) to try and precent the formation of varices
27
What annual screening should be done with cirrhosis pts?
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
What is the management of ascites?
``` 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
Refractory ascites
ascites that doesn't respond to our treatment poor prognosis
30
What is the treatment for hepatic encephalopathy?
restrict dietary protein in diet lactulose (nonabsorbable sugar) Rifaxamin or neomycin (nonabsorbale ABX)
31
Lactulose
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
Hepatorenal syndrome
NOT DONE HERE
33
What is primary biliary cirrhosis?
PBC | idiopathic autoimmune of INTRAhepatic small bile ducts thus decrease bile salt excretion
34
Who gets PBC?
middle aged (40-60) age WOMEN
35
I GET SMASHED
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
What is the difference between zone 1 and zone 3 of the liver?
Based on oxygenation Zone 1 - around the portal veins --most oxygenated blood Zone 3 - around the central vein --least oxygenated blood
37
Where is albumin made?
liver | liver is the ONLY source of albumin
38
What is happening to bilirubin in the liver?
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
Will you see higher conjugated or unconjugated bilirubin in cholestasis?
higher conjugated bilirubin the liver is still turning UCB to CB the gallbladder is just having a build up of CB
40
Will you see higher conjugated or unconjugated bilirubin in hepatitis?
higher UCB problem at the site of the liver the UCB is getting to the liver just not getting formed into CB
41
What are major causes of jaundice in adults?
Prehepatic - inherited disorders like Gilberts Hepatic - cirrhosis hepatitis Biliary tree - obstruction
42
What is the initial test of choice for bile duct obstruction like cholestasis?
US
43
What is the difference between collagen types in a normal liver vs a cirrhotic liver?
Normal liver is mainly collagen type 3 Cirrhotic liver is mainly collagen type 1 (best seen with reticulin stain)
44
Why do some pts experience a pruritic rash with cholestasis?
more commonly in chronic cholestasis this is because bile acid cant get out and accumulates in the blood
45
What might steatorrhea tell you?
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
Prehepatic causes of portal HTN
portal vein thrombosis
47
Hepatic causes of portal HTN
Sinusoidal -cirrhosis
48
Posthepatic causes of portal HTN
outflow obstruction like cor pulmonale
49
What is normal HVWP?
Hepatic venous wedge pressure HVWP - IVC = < 4mmHg cirrhosis >4mmHg really bad if its >12mmHg
50
What is a major and potentially life threatening complication of portal HTN?
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
How can you prophylactically treat pts with risk of esophageal varices?
BB - propranolol
52
How do you treat a bleeding esophageal varices?
variceal band ligation (standard of care)
53
What heme problems might a pt with cirrhosis have?
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
How do you manage ascites?
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
What must you do for a pt with new-onset ascites?
get a sample of the fluid via tapping to confirm transudate and r/o bacterial peritonitis
56
SBP
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
What suggests infection of SBP?
peritoneal tap WBC >500 culture at beside of peritoneal fluid positive urine dipstick for leukocyte esterase
58
What is the treatment for SBP?
IV broad spectrum ABX +/- albumin infusion PO ABX for at risk pts (rifaxamin or norfloxacin)
59
What are common pathogens causing SBP?
E. coli K. pn S. pn
60
What are signs of hepatic encephalopathy? What might you see on EEG?
triphasic slow waves on EEG asterixis mental confusion constructional apraxia fetor (odor of mercaptans)
61
How do you treat hepatic encephalopathy?
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
OLT
orthoptic liver transplantation survival after OLT >80% at 5 years
63
What are the indications of OLT?
evidence of end-stage liver disease expected survival < 1 year clinical decompensation of liver disease
64
What are contraindications of OLT?
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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