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Path E3 > Liver Pancreas GB > Flashcards

Liver Pancreas GB Flashcards

1
Q

Liver synthesizes

A

Serum proteins

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2
Q

What can mask hepatic injury

A

Enormous functional reserve and regenerative capacity

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3
Q

Cirrhosis

A

Fibrosis replacement of normal liver tissue with collagen

  • Diffuse
  • Fibrosis
  • Regeneration hepatocytes
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4
Q

Cirrhosis etiology

A 
EtOH abuse
Viral hepatitis
Non-EtOH steatohepatitis
Biliary Diseae
Iron overload
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5
Q

Iron overload can lead to

A

Hepatocytes death and inflammation

Complications include reduced liver function portal hypertension and increased risk for hepatocellular Ca

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6
Q

Cirrhosis symptoms

A

Non-specific -weight loss weakness etc

Liver failure

Portal Hypertension

  • Ascites
  • Collateral Venous channels
  • Splenomegaly
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7
Q

EtOH pathogenesis

A

Toxin

Nutritional deprivation

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8
Q

Jaundice results from

A

Excess bilirubin

>2 mg/dl

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9
Q

Bilirubin unconjugated

A

Insoluble, toxic

Liver usually conjugates it

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10
Q

Conjugated bilirubin

A

Soluble, nontoxic

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11
Q

Jaundice etiology

A

Overproduction
Reduced hepatocytes uptake
Obstruction of bile flow

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12
Q

Hepatitis

A

Hepatocyte injury that is associated with inflammation

With chronic hepatitis results in scaring

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13
Q

Hepatitis causes

A

Viruses
AI mechanism
Drugs
Toxic agents

Similar patterns of liver injury regardless of causative agent

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14
Q

Viral Hepatitis

A

Hep, A, B, C

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15
Q

Hepatitis A

A 
RNA virus
Benign
Self limited
Fecal->oral
Vaccine available 
2-6 week incubation
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16
Q

Hepatitis B

A 
DNA virus
Parenteral contact/sexual spread
4-26 week incubation
Most self limited infection
Increased risk of hepatocellular carcinoma
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17
Q

Hepatitis B can result in carriers

A

Chronic liver diseases, cirrhosis

Vaccine 95% protective Ab response

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18
Q

Hepatitis C

A

RNA virus
Parenteral contact/sexual spread
7-8 week incubation, acute phase asymptomatic
No vaccine

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19
Q

Hallmark features of Hepatitis C=

A

Persistent infection + Chronic hepatitis

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20
Q

Hepatitis C treatment

A

Protease and nucleoside inhibitors

Combination drugs: harvoni

  • Curative in most patients
  • Very expensive
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21
Q

Acute Viral Hepatitis

A

Resolution 8 weeks

Symptoms: none

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22
Q

Acute Viral Hepatitis: Fulminant

A

Massive necrosis that results in acute liver failure, can transition to a chronic state

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23
Q

Chronic Hepatitis

A

Abnormal function for > 6 weeks

24
Q

Alcohol Liver Disease

A

60% of chronic liver disease associated with overuse

40-50% of deaths due to cirrhosis

25
3 main features of alcohol liver disease
Hepatic steatosis (fatty liver) Alcoholic hepatitis Cirrhosis
26
Alcohol liver recovery
Once cirrhosis achieved usually cant go back Steatosis and hepatitis can usually return to normal
27
Hemochromatosis
Iron accumulation in liver pancreas heart AR, chromosome 6
28
hemochromatosis secondary overload
Excessive iron intake
29
Hemochromatosis treatment
Phlebotomy | Fe, chelators
30
Wilson’s Disease
Copper accumulation in liver brain eyes AR
31
Wilson’s Disease treatment
Chelation: D-penicillamine
32
Bile Duct Carcinoma
Cholangiocarcinoma, arises in bile ducts inside and outside of liver, very aggressive but asymptomatic until late stage
33
Hepatocellular Adenoma
Benign | Assocaited with oral contraceptives if discontinued may regress
34
Hepatocellular Adenoma presentation
Acute abdomen | Intra-abdominal bleed
35
Hepatocellular Adenoma
Bland hepatocytes and no bile ducts
36
Fibrolamellar Carcinoma
Distinct from HCC Younger patients 20-40
37
Metastatic Tumros
Often multiple nodules Any primary-GI, Lung, Breast Mets more common than primary tumors
38
Cholelithaisis
Common Most gallstones silent Association with inflamed gallbladder 80% cholesterol stones, 20% pigment stones
39
Choliethiaisis pathogeneis
Supersaturation Initiation Growth
40
Choelithaisis Stone types
Cholesterol mostly radiolucent Bilirubin mostly radiopaque
41
Cholesterol Stones
Whites females | Estrogens
42
Pigment stones
Hemolysis GI disorders Biliary infection
43
Cholecystitis
Acute - Sever RUQ pain - Chemical bacterial reflux ischemia Chronic - Vague symptoms - Stones - Fibrosis and inflammation
44
Carcinoma Gallbaldder
White females 95% associated with stones 5th most common GI malignancies
45
Most common GI malignancy
Colon cancer
46
Functions of Pancreases
Endo and Exocrine
47
Endocrine pancreas
Regulates glucose homeostasis via insulin and glucagon
48
Exocrine pancreas
Critical for food digestion | Pancreatic enzymes include amylase trypsin and chymotripsin and lipase
49
Acute Pancreatitis
Release of lipases, inflammation proteolysis Necrosis of vessels with hemorrhage Fat necrosis
50
Acute pancreatitis elevated enzymes
Amylase | Lipase
51
Chronic Pancreatitis
Progressive destruction exocrine pancrease later stages lose endocrine
52
Chronic Pancreatitis is _____
Irreversible
53
Chronic Pancreatitis morphology
``` Reduced acini Chronic inflammation Fibrosis Obstruction ducts Spare islets ```
54
Pancreatic Exocrine Tumors
Cysts - congenital - pseudonyms - neoplastic cysts
55
Pancreatic Exocrine Tumors carcinoma
Mostly Adenoma
56
Pancreatic Carcinoma
Silent growth Adjacent at Dx Most die within 6 months Smoking doubles risk Also increased risk with diabetes mellitus and chronic pancreatitis

Path E3 (8 decks)

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