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SRNA3AdvancedPatho2 > Exam 3 Liver Disorder > Flashcards

Exam 3 Liver Disorder Flashcards

1
Q

The liver is

A

Largest solid internal organ 1600g (3.5 lbs)

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2
Q

Falciform ligament divides into

A

R and L lobes (abd. wall)

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3
Q

Round ligament is the

A

“ Ligamentim Teres” (umbilicus)

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4
Q

Coronary ligament

A

diaphragm

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5
Q

Liver receives

A

25% of C.O.

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6
Q

How much blood comes from the Hepatic artery?

A

400ml from Hepatic Artery

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7
Q

How much blood comes from the Hepatic Portal vein

A

1000ml from Hepatic Portal Vein

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8
Q

Liver is covered by the

A

Covered by “Glisson capsule” –painful when distended in disease/inflammation

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9
Q

Filters blood for infections

A

Kuppfer cells, NK cells)

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10
Q

Liver and toxins

A

Neutralizes toxins

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11
Q

Liver and Bilirubin

A

Metabolizes Bilirubin from heme

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12
Q

Liver metabolizes nutrients

A

(Protein deamin.NH3 to Urea)

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13
Q

Liver and clotting

A

Synthesizes Prothrombin& clotting factors 7,9,10

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14
Q

Liver and hormones

A

Synthesizes Hormones(angiotensinogen, thrombopoietin, IGF-1, hepcidin)

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15
Q

Liver and cholesterol

A

Synthesizes Cholesterol, lipids, lecithin

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16
Q

Liver and bile

A

Synthesizes bile

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17
Q

Liver Stores:

A

Glycogen
Fe
Cu
Vit.A, K, E, D, B12

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18
Q

**Acute Liver Failure

Leading cause

A

Severe impairment or necrosis of liver cells without preexisting liver disease or cirrhosis

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19
Q

Pathophysiology of Acute Liver Failure (HPN)

A

Hepatocyte edema
Patchy areas of necrosis and inflammatory cell infiltrates disrupt parenchyma.
Necrosis irreversible.

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20
Q

**Acute Liver Failure

Clinical/lab manifestations AVAPHC RAP

A 
Anorexia
Vomiting
Abdominal pain
Progressive jaundice
Hypoalbuminemia
Coagulopathy
Renal dysfunction 
Altered Mental Status
Prolonged Prothrombin Time
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21
Q

**Portal Hypertension

A

Abnormally high blood pressure in the portal venous system / Increase to at least 10 mmHg (normal = 3 mmHg)

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22
Q

**Signs and symptoms of portal HTN (HAC)

A

Hematemesis, Ascites, Caput medusae

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23
Q

**Portal Hypertension-Types Three Types:Pr

A

Prehepatic Intrahepatic Post-hepatic

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24
Q

**Portal Hypertension-Types

Three Types: Prehepatic

A

Portal vein thrombosis

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25
Q

**Portal Hypertension-Types

Three Types: Intrahepatic

A

Fibrosis: cirrhosis, hepatitis, schistosomiasis (CHS)

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26
Q

**Portal Hypertension-Types

Three Types: Posthepatic

A

Post-hepatic (Hepatic vein thrombosis or Right CHF)

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27
Q

**Portal Hypertension Consequences (HP-VAHS)

A 
Hepatopulmonary Syndrome
Portopulmonary Hypertension
Varices (Lower esophagus, stomach, rectum •Life threatening if ruptured) 
Ascites
Hepatic Encephalopathy
Splenomegaly
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28
Q

***Portal Hypertension : What happens with splenomegaly

A

Splenomegaly ->Thrombocytopenia: (↓thrombopoietin from liver and) platelet sequestration in spleen = Increased risk for bleeding

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29
Q

***Hepatopulmonary Syndrome : liver has

A

Liver has ↑production, or ↓clearance of vasodilators

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30
Q

***Hepatopulmonary Syndrome Pathophysiology

A

Causes V/Q mismatch in lungs

RBCs pass too quickly through lungs to exchange O2 = Hypoxemia and SOB

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31
Q

Perfusion adjustment to changes in ventilation

Response to reduced ventilation

A 
Decreased airflow
Reduced PaO2 in blood vessels
Vasoconstriction in pulmonary blood vessels
Decreased blood flow
Blood flow matches airflow
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32
Q

Perfusion adjustments to changes in ventilation

Response to increased ventilation

A 
Increased airflow
Elevated PaO2 in blood vessels
Vasodilation in pulmonary blood vessels
Increased blood flow
Blood flow matches airflow
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33
Q

***Hepatopulmonary Syndrome

Clinical manifestations:

A
  • dyspnea that worsens moving from recumbent to upright position (“platypnea”)
  • Clubbing of the fingers
  • Spider angiomata
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34
Q

***Portopulmonary Hypertension Portal HTN leads to

A

Pulmonary HTN

Right sided HF

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35
Q

***Portopulmonary Vasoconstrictors and cirrhosis

A

↑↑↑in cirrhosis (endothelin“ET-1”) Causes vasoconstriction in lungs

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36
Q

***Portopulmonary Serotonin normally metabolized

A

Serotonin normally metabolized in liver

bypasses diseased liver in Portal HTN –acts on lungs Causes vascular smooth muscle hypertrophy/hyperplasia

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37
Q

***Mean PA pressure and portopulmonary HTN

A

> 25mmHg (normal ~ 14mmHg) Mean PA >50 contraind. for surgery

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38
Q

***Portal Hypertension Treatment

A

No definite treatment
Beta-blockers help prevent variceal bleeding
Bleeding varices:

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39
Q

***Treatment for bleeding Varices–> PEF

A

Fluid Resuscitation
•prophylactic antibiotics
vasoactive drugs (nonselective β-blockers and terlipressin-reduces portal vein pressure and increases mean arterial pressure (MAP))
•Endoscopic variceal band ligation, compression of the varices with an inflatable tube or balloon, and injection of a sclerosing agent

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40
Q

**Ascites: what is it?

A

Accumulation of fluid in the peritoneal cavity

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41
Q

Most common cause of Ascites

A

Cirrhosis

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42
Q

Clinical manifestations of Ascites

A

Abdominal distention

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43
Q

Ascites Evaluation

A

Serum-ascites albumin gradient (SAAG):

Most specific diagnostic indicator

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44
Q

***•SAAG for Ascites

A

(serum albumin) -(albumin level of ascitic fluid)

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45
Q

•Normal SAAG

A

<1.7

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46
Q

•In cirrhosis, what happens to hydrostatic pressure?

A

hydrostatic press. ↑↑↑= more water pushed out of vasc. space into peritoneum. Albumin doesn’t cross easily, concentrating serum albumin.
•Results in Higher SAAG

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47
Q

Ascites on Respiratory

A

10 –20 L fluid displaces diaphragm Causes dyspnea& ↓lung capacity

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48
Q

Ascites on Renal

A

Affects renal function -leads to H2O retention and dilutional hyponatremia
K+ sparing diuretics used

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49
Q

Ascites Fluid removed?

A

1-2 L removed via paracentesis relieves respiratory distress

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50
Q

**Ascites -> Removing too much fluid too fast

A

relieves pressure on blood vessels = hypotension, shock, death

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51
Q

Overflow theory

A

Renal sodium retention is stimulated by portal hypertension
Causes intravascular hypervolemia, which
overflows or “weeps” into the peritoneal cavity

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52
Q

Underfill Theory

A

Hepatic sinusoidal hydrostatic pressure increases, and plasma oncotic pressure
decreases
Causes weeping of the lymph fluid from the surface of the liver

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53
Q

Peripheral Arterial Vasodilation theory or Forward Theory

PICI

A

Is the synthesis of the overflow and underfill theories
Is the most accepted theory
Portal hypertension and splanchnic vasodilation occurs
Causes fluid transudation and lymph formation, producing ascites

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54
Q

Ascites – Medical Treatment diet

A

Dietary salt restriction

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55
Q

Medication management for Ascites

A

Potassium-sparing diuretics

Strong diuretics, such as furosemide or ethacrynic acid

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56
Q

For dilutional hyponatremia

A

Vasopressin receptor 2 antagonists:

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57
Q

Other additional management for Ascites

A

Possible administration of albumin
Monitor serum electrolytes, especially sodium and
potassium

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58
Q

Ascites – Surgical Treatment

A

Transjugular intrahepatic portosystemic shunt OR

peritoneovenous shunt →For refractory ascites

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59
Q

Ascites: Best treatment option

A

Liver transplant

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60
Q

Hepatic Encephalopathy

A

Blood shunted around failing diseased Liver.

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61
Q

***What happens with hepatic encephalopathy

A

Neurotoxic NH3 from intestinal protein digestion, normally converted to urea by liver, circulates to Brain
disrupting neurotransmission and increases intracranial
hypertension.

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62
Q

***Clinical manifestations of Ascites

SAM PC

A 
◘Personality changes
◘Confusion
◘Memory loss
◘Asterixis (flapping tremor)
◘Stupor, coma, death
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63
Q

Hepatic Encephalopathy Treatment

A

Correct fluid and electrolyte imbalances
Withdraw depressant drugs metabolized by liver
↓ dietary protein intake
↓ intestinal bacteria

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64
Q

Hepatic Encephalopathy and intestinal bacteria

A 
• Neomycin (sterlizes bowel)
• Rifaximin (
↓ intestinal NH3 production/absorption)
• Sodium benzoate &amp;
L-ornithineL-aspartate (detoxify NH3)
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65
Q

Medication to decrease intestinal bacteria: Neomycin action

A

Sterilizes bowel

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66
Q

Medication to decrease intestinal bacteria: Lactulose action

A

prevents NH3 absorption from colon

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67
Q

Medication to decrease intestinal bacteria: Rifaximin action

A

↓ intestinal NH3 production/absorption)

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68
Q

Medication that decrease intestinal bacteria by detoxifying NH3

A

Sodium benzoate and L-ornithineL-aspartate (detoxify NH3)

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69
Q

What is Jaundice

A

“icterus”Yellow (or greenish) pigmentation of the skin caused by hyperbilirubinemia

70
Q

***Jaundice and bilirubin concentration

A

total plasma bilirubin concentrations >2.5 mg/dL)

71
Q

**Jaundice Causes Extrahepatic

A

obstructed bile flow (gallstones - conjugated bilirubin back flows into liver, then into blood)

72
Q

***Jaundice Causes Intrahepatic

A

Intrahepatic obstruction ( CIRRHOSIS or HEPATITIS - conjugated and unconjugated backflow into blood)

73
Q

***Jaundice Prehepatic cause

A

Excessive bilirubin from hemolytic ds– unconjugated in blood, not H2O soluble, not excreted in urine)

74
Q

**Jaundice: Clinical manifestations (DCYS)

A

◘Dark urine
◘Clay-colored stools
◘Yellow discoloration first in the sclera then skin
◘Skin xanthomas (cholesterol deposits) and pruritus

75
Q

***Hepatorenal Syndrome Pathophysiology

A

◘ Liver ds. causes hypotension = ↓ renal perfusion,
↓GFR and oliguria. Kidney secretes more renin.
◘ Diseased liver fails to remove excess angiotensin &
vasopressin which travel to kidneys causing ↑↑↑vasoconstriction resulting in kidney failure. resulting in kidney failure.(positive feedback loop)

76
Q

***Hepatorenal Syndrome Two types:

A

Type I and Type II

77
Q

***Hepatorenal Syndrome Two types: Type I (ACRO Big)

A

Type I
◘ Acute renal decompensation
◘ Creatinine >2.5 mg/dL
◘ Often fatal

78
Q

Hepatorenal Syndrome Two types: Type II (CCG)

A

◘ Chronic renal decomp.
◘ Creatinine >1.5 mg/dL
◘ GFR <40 ml/min.

79
Q

Hepatorenal Syndrome: Renal failure demonstrating

A

oliguria, hypotension, and peripheral vasodilation as a result of advanced liver disease

80
Q

Usually associated with alcoholic cirrhosis

A

Hepatorenal syndrome

81
Q

***Treatment of Hepatorenal syndrome

MAL

A 
Manage fluid &amp; electrolytes, bleeding, infections, and encephalopathy
Administer systemic vasoconstrictors (α-adrenergic agonistsand terlipressin) and albumin
Liver transplantation (and kidney in some cases)
82
Q

***What is hepatitis

A

Systemic viral disease primarily affects the liver

Hepatitis A B C D, E

83
Q

What is autoimmune hepatitis

A

Autoimmune hepatitis is a disease in which the body’s own immune system attacks the liver and causes it to become inflamed.

84
Q

Hepatitis can cause

A

Can cause liver necrosis, Kupffer cell hyperplasia, and

infiltration of liver tissue by mononuclear phagocytes

85
Q

Hepatitis and bile flow

A

Obstruction of bile flow and impairment of hepatocyte function

86
Q

**Viral Hepatitis

Chronic active hepatitis

A

◘Seen with Hep B & C

◘ predisposition for splenomegaly, cirrhosis & carcinoma

87
Q

***Viral Hepatitis : Fulminant hepatitis

A

◘ complication of B & C
◘Causes widespread hepatic necrosis
◘Is often fatal

88
Q

Viral Hepatitis Phases; Incubation phase

A

Depends on virus

89
Q

Viral Hepatitis: Prodromal (preicteric) phase
and clinical manifestations.
FeMAHP

A

Begins ~2 weeks after exposure; ends with the appearance of jaundice
Clinical manifestations: Fever, malaise, anorexia,
hepatomegaly and pain

90
Q

***Viral hepatitis Highly transmissible: what phase

A

Prodromal

91
Q

***Viral hepatitis : Icteric phase (AJ)

A

◘Acute phase of illness

◘Jaundice, fatigue & abdominal pain

92
Q

***Viral Hepatitis Recovery phase (BSC)

A

Begins with the resolution of jaundice
Symptoms resolve after several weeks
Chronic or chronic active hepatitis may develop

93
Q

***Viral Hepatitis Recovery phase (BSC)

A

◘Begins with the resolution of jaundice
◘Symptoms resolve after several weeks
◘Chronic or chronic active hepatitis may develop

94
Q

Viral Hepatitis Treatment activity

A

Rest / Restrict physical activity as needed

95
Q

Viral hepatitis treatment DIET

A

Maintain a low-fat, high-carbohydrate diet if bile flow is obstructed

96
Q

Viral hepatitis avoid

A

Avoid direct contact with blood/body fluids of individuals with hepatitis B or C

97
Q

**Hepatitis A Transmission:

A

fecal-oral route

98
Q

**Hepatitis A Risk factors: c

A

rowded, unsanitary conditions

99
Q

Acute but self-limiting infection

A

Hepatitis A

100
Q

No carrier or chronic state with this one

A

Hepatitis A

101
Q

Vaccine Available for which hepatitis (s)

A

Hepatitis A, B

102
Q

**Prevention of Hepatitis A

A

Handwashing

Immunoglobulin before exposure or early in incubation

103
Q

***Hepatitis B Transmission:

A

blood, body fluids
Maternal transmission occurs if the mother is infected
during the third trimester

104
Q

Hepatitis B carrier state

A

50% of cases asymptomatic but contagious due to

carrier state

105
Q

**Hepatitis B Vaccine

A

◘Vaccine available

◘Immunoglobulin provides post-exposure prophylaxis

106
Q

**Hepatitis C: is the (MI)

A

Most common type transmitted by blood transfusion

Is also implicated in infections in pts. w/ IVDA & HIV

107
Q

***Hepatitis C co infection?

A

Co-infection with B is common

108
Q

% of patients developing chronic liver disease

A

80% of cases develop chronic liver disease

109
Q

No vaccine is available

A

Hepatitis C

110
Q

**Hepatitis C management

A

Antiviral medications help control

111
Q

***Hepatitis D

A

Dependent on hepatitis B for replication

Treatment: Pegylated interferon alpha

112
Q

Hepatitis E Transmission

A

Fecal-oral transmission

Contaminated water or uncooked meat

113
Q

Hepatitis Most common in Asian and African countries

A

Hepatitis E

114
Q

Common in developing countries

A

Hepatitis E

115
Q

Hepatitis E vaccine

A

Vaccine in China but not in other countries

116
Q

Hepatitis - Autoimmune: Definition

A

Rare, chronic, and progressive T cell–mediated

inflammatory liver disease

117
Q

Clinical manifestations of Hepatitis- Autoimmune

A

◘ Asymptomatic until icteric phase

◘ Jaundice, fatigue, loss of appetite, and amenorrhea

118
Q

Treatment of Hepatitis- autoimmune

Drugs? What is common with tx withdrawal.

A

Immunosuppressive drug therapy (e.g., corticosteroids or in combination with azathioprine) with remission within 24 months
Relapses common with treatment withdrawal

119
Q

What is cirrhosis

A

Irreversible inflammatory fibrotic disease

Disrupts liver function and liver structure.

120
Q

Most common causes of Cirrhosis

A

alcohol abuse AND viral hepatitis.

121
Q

*****Cirrhosis Pathophysiology (DBB)

A

Damaged tissue regenerates with nodules & fibrosis.
Biliary channels become obstructed = portal hypertension.
Blood shunted around liver = hypoxic necrosis.

122
Q

***Alcoholic liver disease: what is it?

A

Oxidation of alcohol causes damage to hepatocytes

123
Q

***Alcoholic fatty liver (steatosis) (FMR)

A
  • ↑ fat deposition secondary to ↓ in fatty acid oxidation and ↑lipogenesis
  • mildest form
  • reversible if drinking stopped
124
Q

Alcoholic hepatitis (steatohepatitis) (ID)

A
  • Is characterized by inflammation

* Degeneration and necrosis of hepatocytes

125
Q

Alcoholic cirrhosis (fibrosis)

A

Toxic effects of alcohol metabolism, immunologic alterations, oxidative stress from lipid peroxidation and malnutrition occur.

126
Q

***Nonalcoholic fatty liver disease

A

Infiltration of hepatocytes with fat w/o alcohol intake

Associated with obesity

127
Q

Biliary Cirrhosis begins where

A

Begins in bile canaliculi and ducts

128
Q

Primary biliary cirrhosis (autoimmune)

A

T-cell and antibody-mediated destruction of small

intrahepatic bile ducts

129
Q

Secondary biliary cirrhosis

A

Obstruction of common bile duct

130
Q

Primary sclerosing cholangitis

A

Chronic inflammatory fibrotic disease of the medium- and large-sized bile ducts outside of the liver

131
Q

Cirrhosis – Fe overload disease

A

Hemochromatosis (autosomal recessive)

132
Q

Cirrhosis Fe overload symptoms occur in

A

Symptoms occur in 40’s

133
Q

Cirrhosis Fe overload is an

A

Increased iron deposits in liver, joints, skin

134
Q

What occurs with Fe overload

A

Bronzing of skin occurs (hemosiderin)

135
Q

Treatment of Cirrhosis Fe Overload

A

Phlebotomy, Chelation, Dietary changes

136
Q

Cirrhosis – Cu overload disease is

A

Wilson’s Disease (autosomal recessive)

137
Q

Wilson’s disease Pathology

A

Cu excretion for bile production is defective

Cu builds up in liver

138
Q

Clinical manifestations of Wilson’s disease

A

Hepatic dysfunction, fatigue, jaundice

Kayser-Fleischer ( Cu ring in eye)

139
Q

Treatment of wilson’s disease

A

Treatment w/ chelation (penicillamine)

140
Q

A person has alcoholic liver disease. What is
the sequence for the development of this
disease?

A
  1. Incubation, prodromal, icteric, and recovery
  2. Prehepatic, intrahepatic, and extrahepatic
    * *3. Steatosis, steatohepatitis, and fibrosis
  3. Overflow, underfill, and peripheral artery vasodilation
141
Q

Cholecystitis

A

Inflammation of the gallbladder

Acute vs chronic

142
Q

Cholecystitis Clinical manifestations

A

• RUQ pain, Fever, leukocytosis, rebound tenderness

143
Q

Treatment of Cholecystitis FARP

A

Pain control
Replacement of fluids / electrolytes
Fasting
Antibiotic administration

144
Q

Cholecystitis and emergent

A

Perforated gallbladder: Immediate cholecystectomy

145
Q

Cholelithiasis and symptoms

A

Gallstone obstruction

Many individuals have them but are asymptomatic

146
Q

***Risk factors for Cholelithiasis

A 
Rapid wgt. loss
Obesity
Middle age,
Female gender, 
Oral contraceptives
Pancreatic ds.
147
Q

***Cholelithiasis Two types of stones:

A

Cholesterol: From cholesterol supersaturated bile
Pigmented: Calcium bilirubinate polymer

148
Q

***Clinical manifestations of Cholelithiasis (EJI )

A

Epigastric & RUQ pain
• Intolerance to fatty foods
• Jaundice: Stone in the common bile duct

149
Q

***Cholelithiasis and Biliary colic

A

Lodging of stones in the cystic or common duct

150
Q

• Abdominal tenderness and fever indicates

A

Cholecystitis

151
Q

***In cholelithiasis, When pressure builds against the distended wall of the gallbladder

A

There is a decrease in blood flow. This can result in necrosis,ischemia, and gallbladder perforation.

152
Q

***Treatment of cholelithiasisi

Preferred treatment

A

• Laparoscopic cholecystectomy:

153
Q

Cholelithiasis Large stones: Treatment

A

Lithotripsy

154
Q

Rapidly advancing Cholelithiasis tx

A

• Transluminal endoscopic surgery:

155
Q

2 other treatments for cholelithiasis

A

• Endoscopic retrograde cholangiopancreatography and

sphincterotomy with stone retrieval

156
Q

Cholelithiasis Alternative treatment: Drugs that dissolve smaller stones such as

A

Bile acid chenodeoxycholic acid (CDCA) and ursodeoxycholic acid
• Ursodiol

157
Q

Liver Transplant

Three Phases in Liver Transplant surgery: DAN ILN

A

◘ Dissection Phase →Incision for access
◘ Anhepatic Phase→ Liver isolated from circulation
◘ Neohepatic Phase→ New liver reperfused

158
Q

**Anhepatic Phase (THD)

A

◘ Trial clamping of IVC 30-60 seconds.
◘ Hypotension usually ensues as the vena cava is cross-clamped due to a 50-60% reductionin venous return. Determine pt’s ability to withstand drop in preload.

159
Q

**Neohepatic Phase

A

Most hemodynamic instability in this phase secondary to reperfusion of the portal vein -
Causes DROP in the systemic vascular resistance
even greater than that seen with vena cava crossclamp.

160
Q

During neohepatic phase what indicates graft function ?

A

Decrease in C.O. and increase in SVR indicates graft
is functioning correctly and new liver is beginning
to metabolize vasoactive substances that produce
the characteristic low SVR and high C.O. in pts with
end stage liver disease.

161
Q

Liver Transplant Coags:

A

◘FFP to maint. INR <1.5
◘Platelets to maint. count >50k
◘Cryoprecipitate to maint. Fibrinogen >150mg/dl

162
Q

Liver transplant: What is MELD?

A

Model for End stage Liver Disease

163
Q

The MELD uses (CIBN)

A

Creatinine,
INR
Bilirubin and Na to predict risk of mortality in pt.s with end-stage liver disease.

164
Q

MELD Score of 25 =

A

30 day mortality rate of 50% in pts. undergoing abd. Surgery

◘6 (mild illness) to 40 (severe illness

165
Q

Anesthesia Considerations for liver pts undergoing general surgery→Pts with chronic alcohol ingestion usually have

A

increased anesthetic requirements (MAC) for isoflurane (due to cross-tolerance).

166
Q

Anesthesia Considerations for liver pts undergoing general surgery

A

Hepatic clearance of muscle relaxants must be
considered in pts with cirrhosis. Succinylcholine or
mivacurium are acceptable – but their actions may be
prolonged in pts with severe liver ds.

167
Q

Anesthesia Considerations for liver pts undergoing general surgery Glucose peri-op____
Avoid______

A

may be needed for hypoglycemia

Avoid esophageal instrumentation in pts with varices

168
Q

Anesthesia Considerations for liver pts undergoing general surgery→ What may be sufficient to provide analgesia and amnesia in critically ill pts. with acute liver failure undergoing surgery to correct life-threatening problem?

A

Low dose volatile anesthetics or even nitrous oxide

alone

169
Q

Anesthesia Considerations for liver pts undergoing general surgery→Administer

A

Blood slowly to minimize risk of citrate intoxication (if infused too quickly could result in ↓Ca++ and ↓Mg++)

170
Q

Describe the 3 main paths of blood flow in liver.

A

Hepatic vein
Right and Left hepatic arteries
Portal vein

171
Q

Treatment of Acute liver failure (NABL)

A

N-acetylcysteine:For acetaminophen poisoning
Antiviral therapy (↑ survival rate in cases of viral hepatitis)
↓ blood ammonia levels
Liver transplantation

172
Q

Explain the importance of protein metabolism in the liver and the consequences it could have on the body if compromised.

A

The loss of hepatic regulation of protein metabolism is what leads to a rapid death in acute liver failure,4 and that changes in protein metabolism play a role in complications of chronic liver failure such as the development of HE, ascites and last but not least, PCM.

SRNA3AdvancedPatho2 (15 decks)

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