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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
Q

3 main features of alcohol liver disease

A

Hepatic steatosis (fatty liver)

Alcoholic hepatitis

Cirrhosis

26
Q

Alcohol liver recovery

A

Once cirrhosis achieved usually cant go back

Steatosis and hepatitis can usually return to normal

27
Q

Hemochromatosis

A

Iron accumulation in liver pancreas heart

AR, chromosome 6

28
Q

hemochromatosis secondary overload

A

Excessive iron intake

29
Q

Hemochromatosis treatment

A

Phlebotomy

Fe, chelators

30
Q

Wilson’s Disease

A

Copper accumulation in liver brain eyes

AR

31
Q

Wilson’s Disease treatment

A

Chelation: D-penicillamine

32
Q

Bile Duct Carcinoma

A

Cholangiocarcinoma, arises in bile ducts inside and outside of liver, very aggressive but asymptomatic until late stage

33
Q

Hepatocellular Adenoma

A

Benign

Assocaited with oral contraceptives if discontinued may regress

34
Q

Hepatocellular Adenoma presentation

A

Acute abdomen

Intra-abdominal bleed

35
Q

Hepatocellular Adenoma

A

Bland hepatocytes and no bile ducts

36
Q

Fibrolamellar Carcinoma

A

Distinct from HCC

Younger patients 20-40

37
Q

Metastatic Tumros

A

Often multiple nodules

Any primary-GI, Lung, Breast

Mets more common than primary tumors

38
Q

Cholelithaisis

A

Common
Most gallstones silent
Association with inflamed gallbladder

80% cholesterol stones, 20% pigment stones

39
Q

Choliethiaisis pathogeneis

A

Supersaturation
Initiation
Growth

40
Q

Choelithaisis Stone types

A

Cholesterol mostly radiolucent

Bilirubin mostly radiopaque

41
Q

Cholesterol Stones

A

Whites females

Estrogens

42
Q

Pigment stones

A

Hemolysis
GI disorders
Biliary infection

43
Q

Cholecystitis

A

Acute

  • Sever RUQ pain
  • Chemical bacterial reflux ischemia

Chronic

  • Vague symptoms
  • Stones
  • Fibrosis and inflammation
44
Q

Carcinoma Gallbaldder

A

White females

95% associated with stones

5th most common GI malignancies

45
Q

Most common GI malignancy

A

Colon cancer

46
Q

Functions of Pancreases

A

Endo and Exocrine

47
Q

Endocrine pancreas

A

Regulates glucose homeostasis via insulin and glucagon

48
Q

Exocrine pancreas

A

Critical for food digestion

Pancreatic enzymes include amylase trypsin and chymotripsin and lipase

49
Q

Acute Pancreatitis

A

Release of lipases, inflammation proteolysis

Necrosis of vessels with hemorrhage

Fat necrosis

50
Q

Acute pancreatitis elevated enzymes

A

Amylase

Lipase

51
Q

Chronic Pancreatitis

A

Progressive destruction exocrine pancrease later stages lose endocrine

52
Q

Chronic Pancreatitis is _____

A

Irreversible

53
Q

Chronic Pancreatitis morphology

A 
Reduced acini
Chronic inflammation
Fibrosis
Obstruction ducts
Spare islets
54
Q

Pancreatic Exocrine Tumors

A

Cysts

  • congenital
  • pseudonyms
  • neoplastic cysts
55
Q

Pancreatic Exocrine Tumors carcinoma

A

Mostly Adenoma

56
Q

Pancreatic Carcinoma

A

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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