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GI: Clin Med IIA > Disorders of the liver part 1 > Flashcards

Disorders of the liver part 1 Flashcards

1
Q

hepatocytes receive blood from what 2 sources?

A
  1. Oxygenated blood from hepatic arteries
  2. Venous blood from portal vein (which carries nutrients from GI tract)
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2
Q

what do hepatocytes do?

A
  1. “Filter” blood and put back into general circulation through hepatic veins
    - Filter and store nutrients - vitamins, iron, copper
    - Filters and converts “wastes” to be excreted - Converts ammonia to urea to be excreted by kidneys; Drugs and alcohol
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3
Q

what two processes in th eliver are responsible for Blood glucose management

A
  1. Glycogenesis
    - Converting glucose to glycogen - stored in liver
  2. Glycogenolysis
    - Converting glycogen, fats & proteins to glucose
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4
Q

4 physiologies that happen in the liver

A
  1. blood glucose management
  2. Synthesis of cholesterol for use as bile salts and steroid hormones
  3. Synthesis of plasma proteins (albumin) and clotting factors
  4. Produces bile (conjugated bilirubin, water, bile salts, & cholesterol)
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5
Q

how does the liver make Testosterone

A

Synthesis of cholesterol for use as bile salts and steroid hormones

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6
Q

what serves as digestive enzyme AND removal vehicle for bilirubin and excess cholesterol

A

Bile

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7
Q

common manifestations of liver disease

A
  1. Hyperbilirubinemia
  2. Jaundice
  3. coagulopathy
  4. Thrombocytopenia
  5. Thrombocytopenia, Leukopenia, Anemia
  6. Hypoalbuminemia
  7. Portal HTN
  8. ascites
  9. Spontaneous bacterial peritonitis
  10. Hepatorenal Syndrome
  11. pruritis
  12. Testicular atrophy, gynecomastia (males); Menstrual irregularities (females)
  13. Spider nevi & Palmar Erythema
  14. Hepatic Encephalopathy
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8
Q

what manifestation results from the accumulation of bilirubin in body tissues
A product of heme metabolism

A

jaundice (icterus)

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9
Q

T/F: When ordering, you generally order total and direct bilirubin for liver disease

A

T

Total Serum bilirubin = 0.2-1.2 mg/dL
Total Direct Bilirubin = < 0.3 mg/dL

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10
Q

Increased Unconjugated bilirubin in serum
D/T increased RBC hemolysis
Impaired uptake d/t certain illness
No/little effect on conjugated serum bilirubin

what is this manifestation

A

Pre-Hepatic Jaundice

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11
Q

two types of hepatic jaundice

A
  1. Increased Unconjugated bilirubin in serum - Impaired function of hepatocytes
  2. Increased Conjugated bilirubin in serum - Hepatocellular inflammation obstructs flow to hepatic ducts - blocking excretion
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12
Q
  1. Increased Conjugated bilirubin in serum
    - Obstruction in biliary tract blocking excretion
  2. No/Little effect on unconjugated bilirubin
  3. Decreased bilirubin in gut
    - Pale stools
    - No urobilinogen in urine

what is this manifestation

A

Post Hepatic Jaundice

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13
Q

Stool and urine color are normal
Mild jaundice
No bilirubin in the urine.
Splenomegaly occurs in all hemolytic disorders except in sickle cell disease.

what type of hyperbilirubinemia is this

A

Unconjugated Hyperbilirubinemia

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14
Q

Pruritus and jaundice
Light-colored stools
Malaise, anorexia, low-grade fever, and right upper quadrant discomfort Dark urine
Hepatomegaly, spider telangiectasias, palmar erythema, ascites, gynecomastia, sparse body hair
ALL depend on the cause, severity, and chronicity of liver dysfunction.

what is this hyperbilirubinemia

A

Conjugated Hyperbilirubinemia

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15
Q

Hyperbilirubinemia ma be d/t abnormalities in the:

A

Formation
Transport
Metabolism
Excretion of bilirubin

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16
Q

how is Thrombocytopenia, Leukopenia, Anemia
manifestations of liver disease?

A
  • Hematopoietic Stimulators - Thrombopoietin, Erythropoietin (Kidney and Liver)
  • Bone Marrow Suppression - Viral hepatitis, Excess alcohol consumption, Medications used to treat cirrhosis
  • Diminished “filtering” of blood and absorption from GI
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17
Q

how is coagulopathy a manifestion of liver disease

A
  • Decreased production of clotting factors - Except III, IV, and VIII
  • Decreased absorption/storage of Vitamin K - Needs the presence of bile to be absorbed from GI tract
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18
Q

how does thrombocytopenia happen in liver disease

A
  • Liver produces thrombopoietin (TPO) needed to stimulate thrombopoiesis
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19
Q

how is portal hypertension a manifestation of liver disease

A
  1. Increase in pressure within the portal vein
    - Vein that carries blood from digestive organs to liver
  2. The increase in pressure is caused by a blockage in blood flow through liver
  3. Increased pressure causes large veins/varices to develop across the esophagus and stomach to get around blockage
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20
Q

MCC of portal HTN

A

cirrhosis - scarring of liver

The scar tissue blocks the flow of blood through the liver and slows its processing functions

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21
Q

gold standard dx of portal HTN

A

obtaining a hepatic venous pressure gradient measurement

Catheter is inserted inside the inferior vena cava, and then inside the portal vein to measure the difference between both pressures.

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22
Q

manifestations of portal HTN

A
  • Splenomegaly
  • Esophageal Varices
  • Hemorrhoids
  • Caput Medusae
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23
Q

Accumulation of fluid in peritoneal cavity
Most common complication of cirrhosis

A

ascites

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24
Q

how does ascites happen

A
  1. “Underfill”
    - Hypoalbuminemia
    - Decreased serum albumin allows shift of fluid out of blood and into peritoneal cavity
  2. “Overflow”
    - Increased pressure in portal venous system and liver lymphatics
  3. Impairment of RAAS
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25
Q

MC pathogen of Spontaneous bacterial peritonitis

A

E. Coli

Bacterial infected ascites

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26
Q

Arterial vasodilation in splanchnic circulation triggered by portal hypertension

A

Hepatorenal Syndrome

  • Increased production of vasodilators (nitric oxide) in splanchnic circulation
  • As hepatic disease becomes more severe, progressive rise in cardiac output and fall in SVR in splanchnic circulation
  • Kidneys become poorly perfused
  • Causes acute renal failure
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27
Q

how does pruritus happen in liver disease?

A

Bile salts that enter blood and tissue as a result of bile backing up from liver impairment.
Bile salts deposit under skin, trigger receptors

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28
Q

how does Testicular atrophy, gynecomastia (males); Menstrual irregularities (females) happen in liver disease

A

Impaired cholesterol synthesis for testosterone
Impaired inactivation of estrogen = excess estrogen

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29
Q

cause of Spider nevi & Palmar Erythema in liver disease

A

excess estrogen

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30
Q

what is Hepatic Encephalopathy

A
  • Build-up of ammonia and other toxic chemicals in bloodstream.
  • Liver can’t remove waste from your body
  • Normally, ammonia is an end product of protein metabolism.
  • Then, ammonia is filtered and converted to urea by the liver for elimination by the kidneys.
  • S/S: Confusion, tremors, coma
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31
Q

Components of Liver Function Testing

A

(LFT’s or Hepatic Panel)
* Total Protein
* Albumin
* Total Bilirubin
* Direct Bilirubin
* Aspartate Aminotransferase (AST) (SGOT)
* Alanine Aminotransferase (ALT) (SGPT)
* Alkaline Phosphatase (ALP)

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32
Q

Other Liver Function Tests:

A

Gamma glutamyl transferase (GGT)
PT/PTT
Cholesterol
BUN
Hepatitis Panel

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33
Q

what do Liver enzymes measure?

A

Damage to liver cells (hepatocytes)
Biliary obstruction (cholestasis)

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34
Q

Tests of hepatic synthetic function

A

Albumin
PT

Serum bilirubin levels

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35
Q

Liver enzymes measured in serum

A
  1. Serum aminotransferases
    - Alanine aminotransferase (ALT)
    - Aspartate aminotransferase (AST)
  2. Alkaline phosphatase (ALP)
  3. Gamma-glutamyl transpeptidase (GGT)
  4. Lactate dehydrogenase (LDH)
  5. 5’-nucleotidase
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36
Q

Liver enzymes that measure damage to hepatocytes:

A

Serum aminotransferases - AST/ALT
Lactate dehydrogenase (LDH)

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37
Q

Significant elevations of these levels are most often associated with hepatocellular damage

A

Aminotransferases (ALT and AST)

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38
Q

which aminotransferase is most specific for the liver

A

ALT

AST also found in heart and skeletal muscle

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39
Q

high levels of aminotransferase (8-25x nml) is indicative of ?

A

Acute liver damage / Acute liver failure - Acute viral hepatitis, Drug-toxin induced liver damage (Acetaminophen toxicity), Ischemic hepatitis

Elevations in chronic liver disease < 8x normal (Alcoholic fatty liver and Cirrhosis)

ALT > AST = Acute process
AST > ALT = Chronic disease

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40
Q

what can elevate levels of LDH

A
  1. Myocardial infarction
  2. Hemolysis
  3. Malignancy
  4. Rhabdo
  5. Rheumatic disorders
  6. PE
  7. Infections
  8. Ischemic hepatitis
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41
Q

Liver enzymes that measure cholestasis (biliary obstruction)

A
  1. Alkaline phosphatase
  2. Gamma-glutamyl transpeptidase (GGT)
    - GGT found in liver and biliary tract
  3. 5’-nucleotidase
    - Enzyme specific to liver
    - Released with cholestasis (disruption in the flow of bile)
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42
Q

Alkaline phosphatase is found in what three areas

A

liver, biliary tract, and bone

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43
Q

Alkaline Phosphatase elevations > 4x upper limit, what does this indicate?

A

Hepatic cholestasis

Elevations < 4x upper limit = Nonhepatic/non cholestatic cause

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44
Q

One of the first enzymes to increase due to obstructive disease

A

Alkaline Phosphatase

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45
Q

The presence of ____ elevation can confirm elevated ALP as hepatic in origin

A

associated GGT

Increased ALP + GGT = Hepatobiliary Obstruction

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46
Q

Found in many tissues (LIVER, pancreas, spleen, brain)
NOT found in bone disease

A

Gamma-glutamyl transpeptidase (GGT)

47
Q

elevated ALP + elevated GGT = ?

A

cholestatic (obstructive) hepatobiliary disease

48
Q

An isolated elevated GGT w/o elevated ALP = ?

A

alcohol or certain medications

49
Q

Tests indicative of hepatocellular damage (intrinsic hepatic disease)

A

Marked elevation of AST/ALT as compared to ALP
Elevated total bilirubin
Elevated direct bilirubin

50
Q

Tests indicative of obstructive disease

A

Marked elevation of ALP as compared to AST/ALT
Elevated GGT
Elevated or normal total bilirubin
Elevated direct bilirubin

51
Q

causes that can change Bilirubin Levels

A
  1. Overproduction of bilirubin - Prehepatic
  2. Impaired uptake, conjugation, or excretion of bilirubin - Intrahepatic
  3. Backward leakage from damaged hepatocytes or bile ducts d/t blockage - Posthepatic
52
Q

Elevated Conjugated/Direct bilirubin = ?

A

hepatobiliary disease

53
Q

Hypoalbuminemia in the setting of other liver test abnormalities = ?

A

liver damage resulting in diminished liver function

Hypoalbuminemia when other liver tests are normal = not a result of liver damage - Poor nutrition/increased excretion by kidneys

54
Q

A prolonged PT can result from ?

A
  • lack of synthesis of clotting factors (diminished liver function) or consumption/damage to clotting factors (drug induced, DIC, genetic disorders, severe bleeding, Vit. K deficiency)
55
Q

A prolonged PT in the absence of other abnormal liver tests = ?

A

not due to diminished liver function

56
Q

cause of Autoimmune Hepatitis

A
  • Chronic disease of unknown cause - Continuing hepatocellular inflammation and necrosis, can progress to cirrhosis
  • circulating auto-antibodies and elevated serum globulin levels
57
Q

autoimmune hepatitis is MC in who?

A

Most common in young to middle age women
Genetic component

58
Q
  • Insidious onset to sudden attack of fulminant hepatitis - Mild, asx presentation to acute liver failure
  • Often precipitated by a viral illness/drug exposure - Exacerbations may occur postpartum
  • healthy appearance but w/ multiple spider nevi, cutaneous striae, acne, hirsutism, and hepatomegaly
  • Extrahepatic features: arthritis, thyroiditis, or associated with other conditions

what is this presentation?

A

Autoimmune Hepatitis

59
Q

labs/dx work-up for autoimmun hepatitis

A
  • AST/ALT elevations - greater than 1.5-50x normal
  • Elevated total bilirubin
  • Positive ANA (Anti-nuclear antibody)
  • atypical perinuclear antineutrophil cytoplasmic antibodies (pANCA)
  • Antibodies to soluble liver antigen (anti-SLA)
  • DX: Liver BX

Co-exists with Primary Biliary Cirrhosis or Sclerosing Cholangitis approximately 10% of patients

60
Q

tx for autoimmune hepatitis

A
  1. Prednisone 30-60 mg qd
    - Tx is response guided: tapered weekly when response shown to maintenance of 10mg
    - + Azathioprine lowers needed dose of steroid
    -18-24 months for resolution
    - Recurrent flares common
    - IV Steroids for severe acute flares
  2. Liver transplant if fail corticosteroid therapy
61
Q

autoimmune hepatitis can progress to ?

A

cirrhosis

62
Q

what meds can cause drug/toxin induced hepatitis

A
  • Acetaminophen - esp with alcohol
  • Isoniazid - esp with Rifampin
  • Abx - Tetracyclines
  • “Herbal supplements”
63
Q

presentation of Drug/Toxin Induced Hepatitis

A
  • Hepatomegaly
  • Jaundice
  • Fatigue, N/V

Can progress to liver failure

64
Q

labs and tx for Drug/Toxin Induced Hepatitis

A
  • Labs: Elevated transaminases (ALT > AST)
  • Tx: stop offending agent; liver transplant if liver failure ensues.
65
Q

Major cause of overdose-related liver failure

A

Acetaminophen

Failure to recognize that acetaminophen is found in more than one medication

66
Q

ingestion of what amount of acetaminophen can cause drug/toxin induced hepatitis

A

> 4g (4000 mg) adults
80 mg/kg kids

67
Q

Patients often manifest N/V, diaphoresis, pallor lethargy, and malaise
Some patients remain asymptomatic
Labs generally normal

what stage of Acetaminophen Induced hepatitis

A

1 (.5-24 hr)

68
Q

Initially, stage I symptoms resolve and patients appear to improve clinically
Worsening of AST/ALT develop
RUQ pain with hepatomegaly and tenderness
PT, bilirubin elevated

what stage of Acetaminophen Induced hepatitis

A

II (24-72 hours)

69
Q

Symptoms of stage I reappear with addition of jaundice, confusion (hepatic encephalopathy)
Marked elevation in hepatic enzymes, hyperammonemia, and bleeding diathesis
AST/ALT levels exceed 10k
Prolonged PT/INR
Hypoglycemia
Hyperbilirubinemia
Acute renal failure

what stage of Acetaminophen induced hepatitis

A

III (72-96 hours)

Death generally occurs in this stage d/t multiorgan system failure

70
Q

If stage III, enter a recovery phase that starts at day four and is usually complete by day 7
Recovery can be slower in severely ill patients
Symptoms and lab values may not normalize for several weeks
When recovery occurs, it is complete; chronic hepatic dysfunction is not a complication

what stage of Acetaminophen induced hepatitis

A

IV (4 days to 2 weeks)

71
Q

how does AKI occur in Acetaminophen induced hepatitis

A

Due primarily to ATN and Cytochrome P-450 isoenzymes in the kidney

72
Q

how to dx Acetaminophen Induced Hepatitis

A
  • Based on measurement of acetaminophen level
  • Plot the serum level versus time since ingestion on an acetaminophen nomogram
  • Treat “above the line”
73
Q

tx for Acetaminophen Induced Hepatitis

A
  1. Activated charcoal if within 1-2 hours of ingestion
  2. Also treat with N-acetylcysteine oral or IV
    - Acts as a hepatoprotective agent
    - Loading dose for 60 minutes, then infusion over 20 hours
74
Q

what is considered excessive alcohol intake in men and women?

A
  • More than 2 drinks a day in men
  • More than 1 drink a day in women - Risk increases when consumed daily for > 10 years

Risk of cirrhosis increases if other associated liver disease or obesity

75
Q

who has a higher risk of developing alcoholic hepatitis

A

women

76
Q

stages of alcoholic liver disease

A
  1. Fatty Liver (Steatohepatitis)
    - asx, Reversible; Hepatomegaly
  2. Alcoholic Hepatitis
    - acute/chronic inflammation and parenchymal damage
    - Symptomatic, RUQ pain, tender hepatomegaly, typically reversible
    - Fatigue, fever, nausea, anorexia, recurrent infections (aspergillosis)
    - Bouts of jaundice
    - Acute on chronic liver failure, which is fatal
    - Often reversible, but important precursor to cirrhosis
  3. Cirrhosis
    - Symptomatic, not reversible
    - End stage liver failure
    - Ascites, abd pain, splenomegaly, fever
77
Q

Higher frequency in patient who consume over ___ alcohol daily for 10 years

A

50g

4 oz 100 proof whiskey
15oz wine
4 12oz beer cans

78
Q

what is Acetaldehyde

A
  1. Alcohol broken down into acetaldehyde
  2. Toxic to your body and liver
    - Can cause damage at the cellular level - Damages cellular DNA and prevents body from repairing
79
Q

labs for Alcoholic Liver Disease

A
  1. Fatty Liver (Steatohepatitis)
    - Mild AST, ALT elevations
    - Anemia (macrocytic)
  2. Alcoholic Hepatitis
    - greater increase in ALT, AST - 2xAST > ALT
    - Elevations in ALP, not more than 3x normal
    - Elevated total bilirubin
    - Leukopenia, Thrombocytopenia d/t direct toxic effect of alcohol on megakaryocyte production
  3. Alcoholic Cirrhosis
    - AST/ALT elevations
    - Elevated Total Bilirubin > 10mg/dL
    - Hypoalbuminemia
    - Prolongation of PT/INR
    - Anemia (iron def. and folate)
    - Late disease - electrolyte abnormalities, elevated BUN/Cr

Often an incidental finding in an asymptomatic patient.

80
Q

imaging for alcholic liver dz

A
  1. CT or US - US only if looking for biliary cause
  2. DX: Liver bx
    - US guided percutaneous biopsy
    - Demonstrates macrovesicular fat and PMN infiltration with hepatic necrosis
81
Q

tx for alcoholic liver disease

A
  1. General
    - Abstinence from Alcohol - Most Important; Fatty Liver reverses with abstinence from alcohol
    - Nutritional support
    - Folic Acid, Zinc, Thiamine supplementation
  2. pharm
    - Methylprednisolone x 1 mth if alcoholic hepatitis
    - Pentoxifylline 400mg TID x 1 mth (vasodilator)
    — Severe alcoholic hepatitis - esp if with hepatorenal syndrome or hepatic encephalopathy
    — Increases blood flow and tissue oxygenation, decreases blood viscosity
82
Q

Unfavorable prognostic factors of alcoholic liver dz

A
  1. Prolonged PT/PTT
  2. Serum bilirubin > 10mg/dL
  3. Hepatic encephalopathy
  4. Azotemia (Acute renal failure - Hepatorenal syndrome)
83
Q

components of Glasgow alcoholic hepatitis score

A

Age, bilirubin, BUN, WBC, PT/PTT

84
Q

A “YES” to how many questions in CAGE is considered clinically significant and patient may have a problem with their alcohol usage

A

2 or more

85
Q

Presence of liver fat (steatosis) when no other causes for secondary hepatic fat accumulation are present

A

Non-Alcoholic Fatty Liver Disease

86
Q

causes of Non-Alcoholic Fatty Liver Disease

A
  • Obesity (in 40% of patients)
  • DM, metabolic syndrome
  • HTG
  • Medications (Amiodarone, diltiazem, tamoxifen, etc)
  • Cushings
  • PCOS
  • Genetic factors
87
Q

two cateogories of non-alcoholic fatty liver disease

A
  • Non-alcoholic Fatty Liver (NAFL) - Hepatic fat/steatosis without inflammation
  • Non-Alcoholic Steatohepatitis - Hepatic fat/steatosis with inflammation

Most patients diagnosed in 40s or 50s
Pathogenesis is not fully clear

88
Q

presentation of NASH

A

Asymptomatic or mild, vague symptoms

  • RUQ discomfort, hepatomegaly
  • Signs of chronic liver disease uncommon
89
Q

labs and dx of NASH

A
  1. Mildly elevated AST/ALT
    - Can differentiate ETOH steatohepatitis from AST/ALT ratio: AST/ALT ratio with NASH <2
  2. CT or U/S
  3. Liver Bx for definitive Dx
90
Q

NASH tx

A
  1. Lifestyle modifications
    - wt loss, exercise
    - Dietary fat restriction
    - Tight glucose control
  2. Hepatitis vaccines
  3. Medications?
    - Vitamin E (antioxidant)
    - Thiazolidinediones (Actos, Avandia) and Metformin - Insulin sensitizing agents
    - Weight loss agents
91
Q

Risk factors of pts with NASH that can progress to cirrhosis

A

Advanced age
White, Male
Obesity
DM

92
Q

causes of cirrhosis

A

Alcoholic Hepatitis
NASH
Chronic Viral Hepatitis
Drug toxicity (Drug/Toxin Induced Hepatitis)
Autoimmune Hepatitis
Hemochromatosis
Other genetic and metabolic disorders

93
Q

MCC of cirrhosis in the US

A

alc
chornic hep C

94
Q

pathophys of cirrhosis

A
  1. End result of hepatocellular injury/distortion of the hepatic architecture
  2. Fibrosis and nodular regeneration throughout the liver
    - Replaces functional hepatocytes with nonfunctioning fibrotic nodules
95
Q

presentation of cirrhosis

A
  1. Typically insidious onset
  2. Weakness, fatigue, sleep disturbances common
  3. Weight loss, anorexia with advanced disease
  4. N/V, abdominal pain - D/t hepatomegaly or ascites
  5. portal hypertension
    - Hematemesis from esophageal varices often first sign
    - Splenomegaly
  6. Skin manifestations
    - Spider angioma, palmar erythema
    - Ecchymosis - late finding
  7. Menstrual abnormalities, erectile dysfunction, gynecomastia
  8. Vitamin & Nutrient Deficiencies - Anemia, Glossitis and cheilosis
  9. Jaundice - More severe late in disease
  10. Ascites, peripheral edema, pleural effusion - Late findings
  11. Recurrent infections
  12. Hepatomegaly
  13. Caput medusae
  14. Encephalopathy and Acute Renal Failure - late
96
Q

labs for cirrhosis

A

Minimal changes early

  • Elevations in AST, ALT
  • Elevations in ALP
  • Elevations in bilirubin
  • Hypoalbuminemia
  • Anemia (macrocytic initially)
  • WBC fluctuations
  • Thrombocytopenia
  • Prolonged PT/PTT
97
Q

dx studies for cirrhosis

A
  1. US - 1st line imaging
  2. Liver bx - definitive dx
    - US guided percutaneous
  3. EGD - evaluate for esophageal varices
98
Q

tx for cirrhosis

A
  1. No cure without liver transplant!!!
  2. AVOID ALCOHOL!!!
  3. Strict dietary management
    - Getting enough protein, low carbs, low sodium
    - Reduce protein intake if hepatic encephalopathy
  4. Nutritional supplements
  5. Vaccinations - HBV, HAV, Influenza, pneumococcal
  6. Medications not typically helpful except
    - Antivirals if chronic Hepatitis C underlying cause
  7. Avoid meds known to be toxic to the liver
99
Q

before a liver transplant for cirrhosis, what must the pt do?

A

Must have abstained from alcohol for at least 6 mo

100
Q

tx of ascites/edema complications from cirrhosis

A
  1. Sodium restriction
  2. Diuretics - Spironolactone (Aldactone) and Furosemide (Lasix)
  3. Paracentesis
  4. Transjugular Intrahepatic Portosystemic Shunt (TIPS)
    - Primary indication for variceal bleeding
    - Shunts blood out of portal system - reducing portal hypertension
    - Studies reveal this decrease in pressure also reduces occurrence of ascites
101
Q

indications for paracentesis of ascites/edema from cirrhosis

A

If new onset
If cannot tolerate diuretics
If ascites causing rsp problems

102
Q

tx for Spontaneous Bacterial Peritonitis from cirrhosis

A
  1. Increasing ascites with:
    - Worsening abdominal pain
    - Fever
    - Leukocytosis
  2. Paracentesis + cx
  3. tx - Cefotaxime 2 gm IV q8-12h x 5-7 d
    - alt: Augmentin or Ceftriaxone
  4. Prophylaxis for recurrent SBP - Oral fluoroquinolones
103
Q

tx for HepatoRenal Syndrome
complication from cirrhosis

A
  1. Azotemia in absence of intrinsic renal disease - Increases BUN and Cr
  2. Hyponatremia, Oliguria common
  3. Two types
    - Type I = Sudden doubling of Cr to a level > 2.5
    - Type II = Slowly progressive
  4. Treatment
    - Stop diuretics
    - Increase blood flow to kidneys
    - IV Albumin
    - Dialysis
    - TIPS
    - Liver transplant
104
Q

tx for hepatic encephalopathy complication from cirrhosis

A
  1. State of disordered cns function resulting from failure of liver to detoxify noxious agents of gut origin b/c of hepatocellular dysfunction
  2. Stages: mild confusion, drowsiness, stupor, coma
  3. CNS drugs can precipitate (Benzos, Opioids)
  4. Diagnosis: clinical suspicion, confirmed with serum ammonia level. No imaging required.
  5. TX:
    - Reduce protein intake
    - Lactulose = limits ammonia forming organisms produced in the gut
    - Rifaximin/Metronidazole - minimize gut ammonia producing bacteria.
105
Q

Anemia and Coagulopathy Treatment from cirrhosis

A
  1. Ferrous sulfate for iron def anemia
  2. Folic acid for folate def anemia (MC alcoholics)
  3. Transfusions if d/t severe blood loss from bleeding varices
  4. Vitamin K for severe coagulopathies
    - Ineffective if no clotting factor synthesis
    - Must give FFP in that case - transient effect - only indicated in circumstances of acute bleeding.
  5. Oral thrombopoietin - possible for thrombocytopenia
106
Q

tx for Esophageal Varices
complication from cirrhosis

A
  1. Present in half of all patients with cirrhosis
  2. Often initial presentation
  3. One third of patients develop significant GI bleed
  4. Diagnosis with EGD
  5. Treatment
    - IV fluids, PRBC’s, FFP (d/t coagulopathy often associated)
    - Octreotide - vasoactive drug/slows bleeding
    - EGD once hemodynamically stable
    - IV abx prophylaxis- Increased risk for infection
    - Procedures - banding; sclerotherapy; balloon tamponade (Associated with more severe complications; Only if cannot stabilize patient or unable to see to perform one of other procedures)
107
Q

Prevention of Rebleeding of esophageal varcies from cirrhosis

A
  • Repeat Band ligation plus Beta blockers (Propranolol)
  • TIPS
  • Liver Transplant

Prevention of any Variceal Bleeding preferred! All with cirrhosis should have EGD to screen for varices.

108
Q

how to determine prognosis of cirrhosis?

A

MELD Score: Model for End Stage Liver Dz

  • Based on bilirubin, creatinine, and INR
  • Used by the United Network for Organ Sharing (UNOS) to prioritize allocation of liver donations
  • MELD = 11.2 log (INR) + 3.78 log (bilirubin) + 9.57 log (creatinine) = 6.43 (Range 6-40)

3 month mortality based on MELD score:

  • 40 or more: 71.3% mortality
  • 30-39: 52.6% mortality
  • 20-29: 19.6% mortality
  • 10-19: 6.0% mortality
  • <9: 1.9% mortality
109
Q

a pt must have a MELD score of ? to qualify for liver transplant

A

14 or higher

110
Q

poor prognostic indicators of Cirrhosis

A
  1. Advanced age
  2. Kidney involvement
  3. DM
  4. Pulmonary involvement
  5. refractory ascites
111
Q

Chronic, autoimmune destruction of intrahepatic bile ducts and cholestasis

A

Primary Biliary Cirrhosis

MC in women ages 40-60
Insidious onset
Genetic component
Often associated with other autoimmune disorders

112
Q

presentation of primary biliary cirrhosis

A
  1. Asx for years - Found incidentally by elevated ALP
  2. Fatigue and pruritus - MC early sx
  3. Later s/sx:
    - Hepatomegaly
    - Xanthomatous lesions
    - Jaundice
    - Steatorrhea
    - Portal Hypertension
    - Other manifestations of cirrhosis
113
Q

labs for Primary Biliary Cirrhosis

A
  1. Early - Elevated ALP and cholesterol
  2. Late - Elevated bilirubin
  3. Antimitochondrial antibodies
  4. (+) ANA and elevated serum IgM

Baseline US completed, liver biopsy not necessary

114
Q

tx for Primary Biliary Cirrhosis

A
  1. Ursodeoxycholic acid - only FDA approved
  • Slows progression of disease
  • Reduces toxicity of cholestasis
  • Can delay or prevent need for liver transplant
  1. Cholestyramine - provide relief of pruritus
  • Binds bile salts
  1. Definitive tx - Liver transplant

GI: Clin Med IIA (12 decks)

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