Liver Flashcards

1
Q

Four stages of cirrhosis

A

1) Compensated. undetectable w/o bx
2) Compensated w/ varices.
3) Decompensated. This is when we start seeing our real symptoms,

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2
Q

Major common complications of cirrhosis (think decompensated)

A

WE DON’T SEE THESE UNTIL LATE STAGE

Ascites
HRS
pHTN
Spontneous bacterial peritonitis
Coagulopathy 
Varices
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3
Q

Biggie causes of cirrhosis

A
HCV
EtOH
HCV and EtOH
Cryptogenic (NAFLD)
HBV
Weird random things like PSC/hemochromatosis/wilson
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4
Q

Symptoms of cirrhosis dt the liver malfunctioning (pHTN, portosystemic shunting, dec detox)

A
Fatigue
Sleep disturbance
Weight loss/wasting
Spider telangiectasis
Caput medusa
Abdominal pain dt liver enlargement
Hematemesis
GYN dysfunction (amenorrhea/ED)
Jaundice
Pruritis
Confusion/AMS
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5
Q

PE findings of cirrhosis

A

LATE.

Appear sick
Palpable liver
SPlenomegaly
Caput medusa
Ascites
Pleural effusion
Jaundice
Derm findings (caput medusa, spider nose)
Esophageal/gastric varices (hematemesis/melena)
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6
Q

Labs for cirrhosis

A

Not until starting to compensate less.

Anemia
WBC low
THrombocytopenia

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7
Q

Imaging for cirrhosis

A

US- liver size/ascites/nodular liver

CT/MRI characterize nodular liver

LIVER BIOPSY IS IMPERFECT GOLD STANDARD. Can indicate etiology. Transjugular approach.

EGD for varices

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8
Q

Use of fibrosure test for cirrhosis

A

Biomarker. Uses 6 serum tests to generate score which is equivalent in predictive value to a liver biopsy in patients with known chronic liver disease!

Kinda cool, we would use this before doing a biopsy. If someone has chronic liver disease and a low fibrosure, this excludes adv cirrhosis. If someone has a high score, then you know it is liver cirrhosis and don’t need to confirm that with a biopsy.

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9
Q

Role of Fibroscan (transient elastography) in cirrhosis

A

Bedside US that measures the liver stiffness/fibrosis.

Can be used to stage the disease & determine if treatment is warranted. Limited by ascites, obesity and severe liver inflammation. Nice idea, not super practical

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10
Q

MELD score in cirrhosis

A

Prognostic scoring system. Measures a mortality risk for pts with end stage liver disease, and useful for predicting short term survival. Also determines where you are on the liver transplant list

Scored from 6->40 made up of lab values that actually has nothing to do with liver

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11
Q

MELD score >26?

MELD Score 16-20?

A

90 day mortality of 85%

90 day mortality of 56%

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12
Q

Level of pHTN that collaterals begin to develop

A

> 10-12mmhg

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13
Q

Sequelae of pHTN

A

Ascites
Varices (eso/gastric)
Hepatic encephalopathy
Splenomegaly/thrombocytopenia dt sequestration.

Beginning of the ned

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14
Q

Ppx tx for variceal bleeding/pHTN

A

Nonselective BB! Nadolol and propranolol!

Reduce portal/collateral blood flow and decrease the portal pressure slightly.

Totally useless once the bleeding starts, but it reduces the first bleed likelihood by 50%

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15
Q

Prehepatic causes of portal HTN

A

Thrombosis/stenosis

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16
Q

Intrahepatic causes of portal HTN

A
Cirrhosis!!!
Hepatitis
Cancer
PSC
Wilson
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17
Q

Post hepatic causes of pHTN

A

Budd chiari
Tumor compression
R sided HF (backflow)
IVC thrombosis (backflow)

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18
Q

Three main causes of ascites

A

Cirrhosis (80%)
Neoplasm
CHF

Protein level will tell you what it is. Elevated protein means it’s not cirrhosis. Same or lower is straight up portal HTN caused

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19
Q

Ascites PE and why it’s innaccurate

A

Need at least 1,500 ml to see it on PE. That’s massive.

Abdominal distention
Bulging flanks
Shifting dullness to percussion
Thrills

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20
Q

Large volume paracentesis amount

A

5-10L

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21
Q

Large volume paracentesis albumin supplementation

A

Supplement 5g of albumin for every liter you tap out over 5L

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22
Q

Two lab values you should get in large volume paracentesis

A

CBC & Cx to r/o SBP

Albumin and total protein to determine etiology

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23
Q

First line therapy for ascites

A

Sodium restriction (<1.5 Na) and fluid restriction (<1.5L) This is for the grade I fluid that is only seen on US

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24
Q

Second line tx for ascites

A

Diuretics. Spironolactone, then furosemide if we don’t see a good enough change. Make sure K is okay

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25
Q

Surgical management for grade III ascites (thrills)

A

Large volume paracentesis (symptomatic relief)

TIPS

liver transplant

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26
Q

Not every patient with wicked bad ascites can get TIPS, why? What criteria do we use?

A

Need MELD <18 and TB <3 (???). Otherwise we’re putting the patient at risk of hepatic encephalopathy and exacerbating the liver dysfunction

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27
Q

Two theories behind hepatic encephalopathy etiology

A

Ammonia buildup, it isn’t being detoxed into urea.

GABA inc NT inhibition

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28
Q

PE signs of encephalopathy

A

Asterixis, twitchiness.

PE signs are just as reliable as getting an ammonia level

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29
Q

Common causes of hepatic enceph

A
SBP
Diuretic therapy
Hypovolemia (ammonia buildup)
Renal failure 
GIB
Constipation (ammonia buildup in gut)
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30
Q

Tx for enceph

A

Lactulose to clear out ammonia

Abx- Xifaxan absorbs ammonia

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31
Q

Most common site of gastroesophageal varices

A

Distal esophagus and proximal stomach. It’s where the IVC and SVC hang out

32
Q

RF for rupturing existing GE varices

A

Anything that increases the pHTN
EtOH
Red marks on varices (seen on EGD, called the red wale sign)
Liver failure

33
Q

Sx of a vairceal bleed

A

Hematemesis/melena/hematochezia
Hemorrhagic shock sx
Liver disease/cirrhosis signs

34
Q

Emergent tx of a variceal bleed

A
pRBC until Hb>7 
NGT w/ lavage
Octerotide (splanchic vasoconstriction)
Balloon tamponade
ENDOSCOPY (banding, sclerotherapy)
35
Q

Endoscopy doesn’t work in a variceal bleed, what now?

A

TIPS! Decompresses the varices.

Can also consider angiotherapy or open surg.

36
Q

Endoscopy for variceal bleed has a lot of treatment options to stop the blood. Let’s talk about them, what’s best?

A

Band ligation has the least rebleeding/complications. But it’s operator dependent, esp during an acute bleed.

Also epi injection
Sclerosant injection
Hemoclipping

37
Q

What is acute hepatitis? What are the two types?

A

Inflammation of the liver.

Infectious etiology (Viral)
Non infectious (AI,  Toxiv, EtOH)
38
Q

Acute hepatitis sx

A

Varies from subclinical to fulminant liver failure.

Fatigue/malaise
Anorexia
N/V
Fever
Enlarged liver
Jaundice
Normal to low WBC
Markedly elevated aminotransferase (>1000)
39
Q

Let’s just talk about hepatitis A

A

Fecal oral transmission. International travel is the leading RF.

Vaccine available
Mortality very low unless pt already has HCV
Anti HAV appears early
Symptomatic tx
Full clinical recovery w/n 3 months
40
Q

IgM indicates ___ disease, whereas IgG indicates _____

A

IgM- active disease

IgG- previous exposure

41
Q

How is HBV transmitted

A

Blood

42
Q

HBV adults/infant recovery discrepancies

A

95% of adults totally recover and have lowkey infections.

90% of infants born with HBV develop acute infection, and of those kids 50% of them develop chronic HBV

43
Q

Exposed to HBV? What do we do

A

HBIG w/n 7 days of exposure followed by HBV vaccination series.

44
Q

Newborns w/ HBV + mom

A

For newborns at risk (mom +) we do a vaginal delivery and give HBIG and HBV vax w/n 12 hours of birth. We’ll also put mom on antiviral therapy during third trimester is the viral load is high

45
Q

HbsAg

A

First evidence of HBV infection. If it persists >6mo, this indicates chronic infection

46
Q

HBV DNA?

A

Active replication :(

47
Q

AntiHBc IgM

AntiHBg IgG

A

Acute hepatitis infection that you’re fighting

IgG indicates chronic or recovered infection

48
Q

HIV/HCV coinfection

A

30%

49
Q

HCV and chronic illness

A

Unlike HBV, 85% of these patients will develop chronic HCV

50
Q

Diagnosing HCV labs

A

HCV RNA PCR serology is confirmatory.

Can also do an ELISA and antiHCV?

51
Q

HCV tx

A

8-12 weeks Harvoni (ledipasvir/sofosbuvir) Takes 3-6 mo for full clinical recovery

52
Q

Hepatitis D is associated with

A

HBV!! Terrible disesae with fulminant hepatic failure/cirrhosis but like you can only get this if you’re actively infected with HBV.

Africa, central asia, eastern europe, amazon

53
Q

Hepatitis E Let’s talk about it

A

Very rare. Fecal oral
Can be spread by pig
No chronic state
Only seen typically in IC patients

54
Q

Autoimune hepatitis, who’s our most common patient? How often does it turn into acute hepatitis?

A

The same patient that gets AI anything. Young to middle aged women.

Despite an insidious onset, this actually turns acute 40% of the time

55
Q

Labs for acute AI hepatitis

A

Aminotransferase >1000
Positive ANA and/or smooth muscle ab
IgG elevated

56
Q

What is needed to establish dx of AI hepatitis

A

Liver biopsy

57
Q

AI hepatitis Tx

A

Corticosteroids. It’s AI silly

58
Q

Is alcoholic hepatitis reversible?

A

Hell yeah!

59
Q

Labs in EtOH hepatitis

A

Macrocytic anemia
Thrombocytopenia (EtOH has a direct toxic effect)
AST/ALT 2:1 & mildly elevated (not >300)
TB elevated
PT/INR elevated

60
Q

Imaging for EtOH hepatitis

A

US- ascites

CT/MRI- moderate/severe steatosis but not inflammation or fibrosis

61
Q

Emergent tx for improving short term mortality for EtOH Hep

A

32mg PO methylprednisone QD for 1 mo if MELD >18

62
Q

Most common drugs that cause drug induced hepatitis

A

MACROBID AND MINOCYCLINE. That’s just because of the widesperad use of them though.

These suckers can cause some problems thru potentiation efx
IND, rifampin, APAP, etOH

63
Q

1/3 of the worlds population has

A

HBV. Mostly from being born with it :(

64
Q

Dominant cause of cirrhosis and HCC

A

HBV

65
Q

How much does HBV inc HCC risk

A

20-30%

Having a high viral load is a predictor of cirrhosis/HCC risk

66
Q

First line for chronic HBV

A

Entecavir/Tenofavir. Lifelong therapy, prevents repliation

67
Q

When do we consider HCV to be chronic

A

> 6 mo of persistent HCV RNA serology

68
Q

HCC is associated with

A

Underlying liver disease. Hepatitis, NASH

69
Q

HCC clinical presentation

A
Insidious until cirrhotic
Weakness, weight loss, anorexia
Ascites
Jaundice, icterus pruritis
Tender enlarged liver
70
Q

HCC WU

A
CBC
CMP
Lipase
PT
Alpha fetoprotein
HCV/HBV testing
Alpha 1 antitrypsin
EtOH
71
Q

Imaging for HCC

A

US

MRI

72
Q

Diagnostic for HCC

A

Biopsy, but 1-3% chance of seeding with needle.

73
Q

Size of tumor and biopsy guidelines

<1cm?
1-2cm?

A

<1cm gets CT/MRI every 3 months to assess for enlarging lesion

1-2? Bx should be performed

74
Q

> 2cm HCC lesion w/ cirrhosis, elevated AFP levels?

A

Manage w/o biopsy. Don’t need the risk, that’s definitely cancer

75
Q

Only long term cure for HCC

A

Surgical. Be it resection or transplant. HCC is radioinsensitive and chemo is ineffective. VEGF blockers have been shown to slow progression.

76
Q

HCC tumor near the hepatic artery?

A

Can try transarterial chemoembolization (TACE) or transarterial radioembolization (TARE)