Liver Cirrhosis Flashcards

1
Q

What is the primary cause of cirrhosis in the Western countries?

A

Alcoholism

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2
Q

What care the three common genetic diseases that can cause cirrhosis?

A

Hemochromatosis, Wilson’s Dz (Copper Overload), Alpha 1 Antitrypsin Deficiency

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3
Q

What is the second most cause of cirrhosis in the Western countries?

A

Metabolic Dz

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4
Q

Other causes of Cirrhosis

A

Hepatitis B and C, Auto-immune Hepatitis, and Sarcoidosis, Drugs, Toxins, Cryptogenic, Biliary Dz, Venous Outflow Obstruction (very uncommon)

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5
Q

Ongoing ________ results in ongoing liver injury and progression of fibrosis with eventual progression to cirrhosis.

A

Inflammation

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6
Q

Liver dz characterized pathologically by loss of the normal microscopic lobular architecture with fibrosis and nodular regeneration.

A

Cirrhosis

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7
Q

I’m looking at a smooth maroon liver in surgery, before doing a histology slide of the cells, what would you think about this liver? What would you expect on a histology slide?

A

Normal Liver, it will look pretty convoluted and meshlike/brainlike

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8
Q

I’m looking at a nodular discolored liver in surgery, before doing a histology slide of the cells, what would you think about this liver? What would you expect on a histology slide?

A

Cirrhotic Liver; You will see large spots with surrounding discoloration, etc.

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9
Q

The type of cirrhosis that is associated with NO signs or symptoms of liver dz

A

Compensated

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10
Q

The type of cirrhosis that is associated with complications/symptoms/signs.

A

Decompensated

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11
Q

When looking at a liver on a CT, noting some scarring and a more “white” image, would indicate?

A

Cirrhosis of the liver causing change in architecture. When compared to normal, this looks shrunken.

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12
Q

Patient with yellow skin, what do you think?

A

JAUNDICE

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13
Q

Patient with yellowing of the eyes is a condition indicative of jaundice is termed?

A

Icteric Sclerae

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14
Q

When the liver is affected, what can happen in male individuals?

A

Gynecomastia

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15
Q

A common finding in patients with liver dz/cirrhosis that is seen as a redness of the hands/palms

A

Palmar Erythema

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16
Q

A common finding in patients with liver dz/cirrhosis that is seen as a localized redness with small vessels.

A

Spider Angioma

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17
Q

A common finding in patients with liver dz/cirrhosis that is seen as an enlarged preauricular “mass.”

A

Parotid Enlargement

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18
Q

A common finding in patients with liver dz/cirrhosis that is seen as a torturous elevated vein of the skin termed

A

Caput Medusa

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19
Q

Define Ascites

A

Swelling of the abdomen where you can note a severe difference of tympany and dullness when percussing. Dullness would be over the “fluid” portion.

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20
Q

Complications of Cirrhosis (8)

A
  1. Portal HTN
  2. Varices and Variceal Bleeding
  3. Hyponatremia
  4. Ascites
  5. Hepatic Encephalopathy
  6. Hepatorenal Syndrome
  7. Hepatopulmonary Syndrome
  8. Hepatocellular Cancer
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21
Q

The portal venous system begins and ends in the ____________.

A

Capillaries

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22
Q

What creates the portal vein?

A

Splenic vein, Superior mesenteric vein, and inferior mesenteric vein.

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23
Q

What is the NORMAL portal vein pressure?

A

5-6 mm Hg

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24
Q

Normal hepatic sinusoids have ______ resistance to flow

A

Low

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25
Q

Cirrhotic liver will _______ resistance, making the pressure ______. This pressure change is what causes _________________ to occur.

A

Create; high; Portal HTN

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26
Q

When is portal HTN “clinically significant”

A

10+ mm Hg

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27
Q

Dilated collateral veins in the portal-systemic circulation, commonly in the gastric or esophageal veins.

A

Varices

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28
Q

When do varices start developing? When do these varices cause bleeding?

A

10+ mm Hg; 12+ mm Hg

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29
Q

Clinical presentation of varices due to portal HTN (since they are internal)

A

Hematemesis, Hematochezia or melena (usually acute)

30
Q

Mortality rates from the first bleeding of esophageal varices is about? (Bleeding risk increases about 4% every year in pts with cirrhosis)

A

25-50% HIGH!!!

31
Q

What is the likelihood of recurrence in esophageal varices rupture without treatment

A

70%

32
Q

If a patient is at high risk for bleeding, what test can you do?

A

Endoscopy

33
Q

Varices develop at a rate of

A

4-12% per year

34
Q

What is the best way to prevent bleeding?!

A

Primary prohylaxis!! The goal is to reduce the portal pressure to less than 12 mm Hg. (Treat underlying cause)

35
Q

What can you give to reduce the portal pressures?

A

Non-selective Beta Blocker (nadolol, propanolol)! Target HR of 50-60 BPM, decrease HR by 25% of baseline

36
Q

It is a procedure in which an enlarged vein or a varix (the plural is varices) in the esophagus is tied off or ligated by a rubber band delivered via an endoscope.

A

Endoscopic Variceal Ligation

37
Q

Disadvantage of the EVL

A

Doesn’t affect the portal pressure, just helps prevent bleeding

38
Q

Risk factors for the first variceal bleed

A
  1. Advanced Cirrhosis
  2. Portal Venous Pressue 12+ mm Hg
  3. Large Varices
  4. Stigmata
  5. Recent stopping of beta blockers
  6. Volume overload
39
Q

How do you dx a variceal bleed?

A

Endoscopy

40
Q

How do you treat the first variceal bleed?

A
  1. Resuscitation
  2. Vasoactive Drug: Octreotide
  3. EGD: Banding or Scleropathy
  4. Rescue Treatment: TIPS
  5. Should be on antibiotics (Cipro 500 mg IV x 7 days)
41
Q

What can cause ascites to occur?

A

Combination of abnormal renal function and alterations in portal and splanchnic circulation.

  1. Kidney Na+ retention
  2. Fluid Retention
  3. Expansion of ECF
  4. Ascites and Edema formation
42
Q

How do you treat refractory ascites?

A
  1. Repeated paracentesis or shunt (TIPS)

2. Liver transplant

43
Q

How do you treat mild to moderate Ascites?

A
  1. Na+ restriction (2g/day)

2. K+ sparing diuretic +/- loop diuretic (Spironolactor and furosemide)

44
Q

How do you treat Large Ascites?

A

Same as mild to moderate. May want therapeutic paracentesis, can consider liver transplant.

45
Q

Spontaneous infection of ascitic fluid without an intra-abdominal source that can have a high mortality rate if not treated. common in about 10-30% of pts with ascited

A

Spontaneous Bacterial Peritonitis

46
Q

How would someone with SBP present?

A

Abdominal Pain, Fever, Encephalopathy, and a Decline in Renal function

47
Q

How do you dx SBP?

A

> 250 mm3 of PMN count in Ascites

48
Q

How do you treat SBP?

A

IV 3rd generation cephalosporin

49
Q

Can occur in cirrhosis and acute liver failure; gut toxins induce acute or recurrent bouts of ________.

A

Encephalopathy (Hepatic)

50
Q

Due to toxins escaping the liver and moving throughout the system, a toxin like ammonia can move to the head causing?

A

Hepatic Encephalopathy

51
Q

What can Hepatic Encephalopathy cause?

A

Chronic low grade cerebral edema

52
Q

A clinical manifestation of hepatic encephalopathy where a patient is not responding would be graded Stage _____ with what mental status?

A

4; Coma

53
Q

A clinical manifestation of hepatic encephalopathy where a patient with asterixis would be graded Stage _____ with what mental status?

A

2; Drowsy

54
Q

A clinical manifestation of hepatic encephalopathy where a patient with muscle rig would be graded Stage _____ with what mental status?

A

3; Somnolent

55
Q

A clinical manifestation of hepatic encephalopathy where a patient with tremors would be graded Stage _____ with what mental status?

A

1; mildly confused with or without inverted sleep patterns.

56
Q

When suspected Hepatic Encephalopathy is present, what would you suspect is causing this?

A
  1. GI Bleeding
  2. Hyponatremia
  3. Infection
  4. CNS medications
  5. Constipation
  6. Non-compliance
57
Q

How do you treat encephalopathy?

A
  1. Lactulose

2. Rifaximin

58
Q

This medication acidifies the colon so that ammonia (NH3) becomes NH4 and cannot be absorbed.

A

Lactulose

59
Q

This medication is a non-absorbable antibiotic used to reduce ammonia producing bacteria in the gut.

A

Rifaximin

60
Q

If a patient has hyponatremia, what should you do!?

A
  1. D/c spironolactone

2. Water restriction – limiting fluid intake to 500-1000 mL/day

61
Q

Impaired renal function in a patient with cirrhosis of the liver, commonly vasoconstriction of the renal circulation.

A

Hepatorenal syndrome (HRS)

62
Q

Dx of HRS

A
  1. Cr > 1.5 or CrCl < 40 mL/mn
  2. Absence of shock, fluid losses, or nephrotoxic drugs
  3. No improvements with diuretic withdrawal and volume expansion
  4. Urine Volume < 500 ml/d
  5. UNa < 10 mEq/L
63
Q

Diffuse Dilation of Pulmonary Arterioles and Alveolar Capillaries

A

Hepatopulmonary Syndrome

64
Q

What else can help you dx Hepatopulonary Syndrome?

A
  1. Bubble Echocardigraphy

2. High shunt fraction (PaO2 < 150 to 200 mm Hg on 100% O2 in the upright position)

65
Q

Over ___ of patients demonstrated improvement in or resolution of the syndrome by 15 months after orthotopic liver transplantation.

A

80%

66
Q

Risk factors the the primary liver cancer (Hepatocellular Carcinoma)

A

HCV > HBV > Other (Alcohol, Hemochromatosis, Cyptogenic)

67
Q

Treatment of Hepatocellular Carcinoma

A
  1. Sx: Liver Transplant or Resection
  2. Local/Regional Therapy (TACE)
  3. Oral Therapy: Sorafenib
68
Q

Testing for ELD (End Stage Liver Disease)

A

Creatinine
Total Bilirubin
INR

69
Q

The higher the number of creatinine, total bili, or INR — indicative of what?

A

Worsening Liver function!

F/u every 3 months

70
Q

In a patient with Liver Cirrhosis, you should check for HCC how often?

A

Every 6 months with AFP and Imaging

71
Q

AFP! Serum alpha-feto protein

A

Can be artificially elevated in certain disease processes and does not indicate HCC(e.g. HCV, testicular cancer, pregnancy). AFP greater than 500 usually diagnostic.