Pancreatic Pathology

Question 1

What is the general definition of pancreatitis?

Answer 1

Inflammation in the pancreas with associated injury to the exocrine parenchyma.

Question 2

What is the range of severity for pancreatitis?

Answer 2

Mild to a life-threatening disease.

Question 3

What are the two main types of pancreatitis?

Answer 3

Acute pancreatitis and Chronic pancreatitis.

Question 4

What is the key difference between acute and chronic pancreatitis regarding parenchymal injury?

Answer 4

Acute pancreatitis involves reversible parenchymal injury, while chronic pancreatitis involves irreversible loss of exocrine pancreatic parenchyma.

Question 5

How is acute pancreatitis specifically defined in terms of injury and inflammation?

Answer 5

Reversible pancreatic parenchymal injury associated with inflammation.

Question 6

What are the two main causes accounting for 80% of acute pancreatitis in Western countries?

Answer 6

Biliary tract disease and alcoholism.

Question 7

Name two metabolic aetiological factors for acute pancreatitis.

Answer 7

Alcoholism and Hypercalcemia (also Hyperlipoproteinemia, certain drugs).

Question 8

Name two mechanical aetiological factors for acute pancreatitis.

Answer 8

Gallstones and Iatrogenic injury (e.g., ERCP or operative injury).

Question 9

What are some genetic factors that can predispose to acute pancreatitis?

Answer 9

Mutations in PRSS1, SPINK1, CASR genes, or Cystic fibrosis (CFTR).

Question 10

Name an infectious agent that can cause acute pancreatitis.

Answer 10

Mumps or Coxsackievirus.

Question 11

What specific drugs are listed as potential causes of acute pancreatitis?

Answer 11

Azathioprine, statins, GLP-1 agonists, DPP-4 inhibitors.

Question 12

What vascular conditions are listed as causes of acute pancreatitis?

Answer 12

Shock, atheroembolism, vasculitis (e.g., polyarteritis nodosa).

Question 13

How does alcohol directly affect pancreatic acinar cells and the Sphincter of Oddi?

Answer 13

Causes direct toxicity to acinar cells and increased tone of the Sphincter of Oddi.

Question 14

What are two other effects of alcohol contributing to pancreatitis (excluding direct toxicity/Sphincter of Oddi)?

Answer 14

Increases calcium levels and promotes activation of pancreatic enzymes (also free radical injury).

Question 15

What are the three main pathogenetic mechanisms of acute pancreatitis?

Answer 15

1. Pancreatic duct obstruction, 2. Primary acinar cell injury, 3. Defective intracellular transport of proenzymes.

Question 16

What is the common endpoint of the pathogenetic mechanisms in acute pancreatitis?

Answer 16

Activation of pancreatic enzymes, leading to destruction of pancreatic parenchyma.

Question 17

How can gallstones or alcohol lead to pancreatic duct obstruction?

Answer 17

Gallstones by impacting the ampulla of Vater; alcohol by increasing sphincter tone and causing protein plugs.

Question 18

What are common causes of primary acinar cell injury in acute pancreatitis?

Answer 18

Viruses (e.g., mumps), drugs, direct trauma, ischemia, or shock.

Question 19

How does increased intrapancreatic duct pressure contribute to acute pancreatitis?

Answer 19

For example, from a neoplasm, it causes duct obstruction.

Question 20

What are the initial and subsequent mechanisms following duct obstruction in the pathogenesis diagram (Page 8)?

Answer 20

Interstitial edema, followed by impaired blood flow and ischemia.

Question 21

What is released from acinar cells upon injury according to the pathogenesis diagram (Page 8)?

Answer 21

Intracellular proenzymes and lysosomal hydrolases.

Question 22

What local effect can result from the accumulation of enzyme-rich fluid and protein plugs in pancreatic ducts (e.g., due to alcohol)?

Answer 22

Local fat necrosis.

Question 23

What are the morphological consequences of protease, lipolytic enzyme, and elastase activation in acute pancreatitis?

Answer 23

Proteases: proteolytic destruction of parenchyma; Lipolytic enzymes: fat necrosis; Elastases: destruction of blood vessels and hemorrhage.

Question 24

Which specific enzyme is responsible for proteolysis in acute pancreatitis?

Answer 24

Proteases.

Question 25

Which specific enzymes are responsible for fat necrosis in acute pancreatitis?

Answer 25

Lipase and phospholipase.

Question 26

Which specific enzyme is responsible for hemorrhage in acute pancreatitis?

Answer 26

Elastase.

Question 27

What is the macroscopic appearance of the pancreas in acute pancreatitis concerning color and necrosis?

Answer 27

Red-black due to hemorrhage, with areas of yellow-white fat necrosis.

Question 28

What is the term for the severe macroscopic form of acute pancreatitis?

Answer 28

Haemorrhagic pancreatitis, characterized by extensive parenchymal necrosis and hemorrhage.

Question 29

Where can macroscopic fat necrosis be observed outside the pancreas in acute pancreatitis?

Answer 29

In the omentum and the mesentery of the bowel, sometimes with calcification.

Question 30

Describe the typical fluid found in the peritoneal cavity in acute pancreatitis.

Answer 30

Serous, turbid, brown-fluid mixed with fat globules.

Question 31

What is the first mechanism listed as responsible for the morphological features of acute pancreatitis (Page 9)?

Answer 31

Acute inflammation.

Question 32

What is the second mechanism responsible for morphological features, involving fluid and vessels (Page 9)?

Answer 32

Vascular leakage and oedema.

Question 33

What are the key microscopic findings in acute pancreatitis regarding inflammation and fat necrosis?

Answer 33

Acute inflammation and focal areas of fat necrosis.

Question 34

How do fatty acids and calcium contribute to the microscopic appearance of fat necrosis?

Answer 34

They combine to form insoluble salts, appearing as a white granular substance.

Question 35

What microscopic changes occur in ducts and islets of Langerhans in severe acute pancreatitis?

Answer 35

Necrosis of ducts and islets of Langerhans, along with enzyme release.

Question 36

What is acute necrotizing pancreatitis characterized by microscopically?

Answer 36

Widespread pancreatic necrosis, including vascular injury and hemorrhage into the parenchyma.

Question 37

Describe the characteristic abdominal pain in acute pancreatitis.

Answer 37

Constant and intense; typically epigastric or referred to the upper back.

Question 38

What are common gastrointestinal symptoms, besides pain, in acute pancreatitis?

Answer 38

Anorexia, nausea, and vomiting.

Question 39

What do Cullen's sign (umbilical bruising) and Grey Turner's sign (flank bruising) indicate in acute pancreatitis?

Answer 39

Retroperitoneal haemorrhage.

Question 40

What is the term 'acute abdomen' referring to in the context of acute pancreatitis?

Answer 40

A clinical presentation of severe abdominal pain requiring urgent evaluation.

Question 41

List three major systemic complications/responses seen in severe acute pancreatitis.

Answer 41

Septic shock/Systemic Inflammatory Response Syndrome (SIRS), Acute Respiratory Distress Syndrome (ARDS), Disseminated Intravascular Coagulation (DIC) (also acute renal failure, leukocytosis).

Question 42

What is a common hematological finding indicating systemic inflammation in acute pancreatitis?

Answer 42

Leukocytosis.

Question 43

Which two serum enzymes are typically markedly elevated in acute pancreatitis, and what are their elevation timeframes?

Answer 43

Serum amylase (first 24 hours) and serum lipase (elevated for 72-96 hours).

Question 44

What electrolyte abnormality can occur in acute pancreatitis and why?

Answer 44

Hypocalcemia, due to precipitation of calcium soaps in areas of necrotic fat (saponification).

Question 45

In what percentage of acute pancreatitis cases might glycosuria be found?

Answer 45

In about 10% of cases.

Question 46

What is the typical outcome for most individuals with acute pancreatitis?

Answer 46

Complete recovery.

Question 47

What is the approximate mortality rate for acute pancreatitis, and when is it often fatal?

Answer 47

About 5%, often fatal during the first week of illness.

Question 48

What are major causes of death in severe acute pancreatitis?

Answer 48

Shock/SIRS, ARDS, and acute renal failure.

Question 49

What is gangrenous pancreatitis, a severe complication of acute pancreatitis?

Answer 49

Necrotic pancreatic debris, often infected by gram-negative organisms from the gut (occurs in 40-60% of severe cases).

Question 50

Name two local complications that can arise from acute pancreatitis.

Answer 50

Pancreatic pseudocyst formation and sterile pancreatic abscess.

Question 51

What is a pancreatic pseudocyst defined as?

Answer 51

A collection of fluid (enzymes, blood, debris) walled off by fibrous/granulation tissue, lacking an epithelial lining.

Question 52

What is a sterile pancreatic abscess?

Answer 52

A collection of liquefied necrotic tissue or pus within/adjacent to the pancreas, without bacterial infection.

Question 53

Can acute pancreatitis progress to another form of pancreatitis?

Answer 53

Yes, it can progress to chronic pancreatitis.

Question 54

How is chronic pancreatitis defined, emphasizing its key irreversible features?

Answer 54

Inflammation of the pancreas with irreversible destruction of exocrine parenchyma and fibrosis.

Question 55

What happens to the endocrine parenchyma in the late stages of chronic pancreatitis?

Answer 55

Destruction of endocrine parenchyma often occurs.

Question 56

What is the prevalence range of chronic pancreatitis?

Answer 56

0.04% to 5%.

Question 57

What is a common initial pathogenetic factor for developing chronic pancreatitis?

Answer 57

Repeated bouts of acute pancreatitis.

Question 58

How does ductal obstruction contribute to chronic pancreatitis pathogenesis?

Answer 58

Obstruction by concretions (calculi) can lead to chronic inflammation and fibrosis.

Question 59

Besides calculi, what else can cause further obstruction of pancreatic ducts in chronic pancreatitis pathogenesis?

Answer 59

Neoplasms.

Question 60

What are the effects of toxins like alcohol and its metabolites on acinar cells in chronic pancreatitis?

Answer 60

Direct toxicity, contributing to acinar cell damage and inflammation.

Question 61

How does alcohol-induced oxidative stress contribute to chronic pancreatitis?

Answer 61

Generates free radicals, leading to acinar cell necrosis, inflammation, and fibrosis.

Question 62

What is the specific consequence of alcohol-induced oxidative stress leading to fibrosis in chronic pancreatitis?

Answer 62

Acinar cell necrosis and inflammation precede the fibrosis.

Question 63

Name two other pathogenetic factors for chronic pancreatitis besides repeated acute attacks and alcohol.

Answer 63

Autoimmune pancreatitis and genetic factors (hereditary pancreatitis).

Question 64

What is the most prominent morphological characteristic of chronic pancreatitis at a tissue level?

Answer 64

Extensive parenchymal fibrosis.

Question 65

How are the pancreatic acini and islets of Langerhans morphologically affected in chronic pancreatitis?

Answer 65

Reduced number and size of acini, with relative sparing of the islets of Langerhans (though they may be embedded in fibrosis).

Question 66

What change is typically seen in the pancreatic ducts morphologically in chronic pancreatitis?

Answer 66

Dilation of the pancreatic ducts.

Question 67

What is the gross consistency of the pancreas in chronic pancreatitis?

Answer 67

The gland is typically hard.

Question 68

What features related to ducts and concretions can be seen macroscopically in chronic pancreatitis?

Answer 68

Extremely dilated ducts and often visible calcified concretions (stones).

Question 69

What is the image on page 21B showing in chronic pancreatitis (with blue arrow)?

Answer 69

A large ductal concretion/protein plug within a dilated duct.

Question 70

What type of inflammatory infiltrate is characteristic microscopically in chronic pancreatitis?

Answer 70

Chronic inflammatory infiltrate (lymphocytes, plasma cells).

Question 71

What changes can occur to the ductal epithelium microscopically in chronic pancreatitis?

Answer 71

It can be atrophic or hyperplastic, and ducts may contain concretions.

Question 72

What are the key microscopic changes to the acinar tissue and stroma in chronic pancreatitis?

Answer 72

Acinar loss and extensive fibrosis.

Question 73

How are the islets of Langerhans often found microscopically in advanced chronic pancreatitis?

Answer 73

Embedded within dense fibrous tissue.

Question 74

Microscopically, what is the fate of islets of Langerhans when embedded in fibrous tissue in chronic pancreatitis?

Answer 74

While relatively spared initially, their function can eventually be compromised.

Question 75

What is a major digestive sequela of chronic pancreatitis due to exocrine insufficiency?

Answer 75

Chronic malabsorption.

Question 76

What endocrine disorder is a common sequela of chronic pancreatitis?

Answer 76

Diabetes mellitus, due to destruction of endocrine parenchyma.

Question 77

What type of pain is a significant and debilitating sequela of chronic pancreatitis?

Answer 77

Severe chronic pain.

Question 78

What cystic lesion can develop as a sequela in about 10% of patients with chronic pancreatitis?

Answer 78

Pancreatic pseudocysts.

Question 79

Chronic pancreatitis, especially which type, increases the risk of developing pancreatic cancer?

Answer 79

Hereditary pancreatitis particularly increases this risk.

Question 80

What is the approximate 20- to 25-year mortality rate associated with chronic pancreatitis?

Answer 80

Around 50%.

Question 81

What is the peak age range for pancreatic carcinoma?

Answer 81

Elderly, typically 60-80 years.

Question 82

How does cigarette smoking impact the risk of pancreatic carcinoma?

Answer 82

It doubles the risk (x2).

Question 83

Name two pre-existing pancreatic conditions that are risk factors for pancreatic carcinoma.

Answer 83

Chronic pancreatitis and Diabetes mellitus.

Question 84

What are two common gene mutations associated with pancreatic carcinoma?

Answer 84

KRAS and TP53 mutations.

Question 85

Name a familial factor or syndrome that increases the risk of pancreatic carcinoma.

Answer 85

Family history of pancreatic cancer, inherited BRCA2 mutations, or Peutz-Jeghers syndrome.

Question 86

Which racial group has a higher incidence of pancreatic carcinoma?

Answer 86

Blacks > whites.

Question 87

List three common general clinical features of pancreatic carcinoma.

Answer 87

Weight loss, anorexia, and generalized malaise (also weakness).

Question 88

What is Trousseau syndrome, seen in some pancreatic carcinoma patients?

Answer 88

Migratory thrombophlebitis.

Question 89

What is thought to cause Trousseau syndrome in pancreatic carcinoma?

Answer 89

Platelet-aggregating factors and procoagulants released from the carcinoma.

Question 90

In approximately what percentage of pancreatic cancer patients does Trousseau syndrome occur?

Answer 90

In about 10% of patients.

Question 91

In which part of the pancreas do approximately 60% of pancreatic cancers arise?

Answer 91

In the head of the pancreas.

Question 92

Where do 15% and 5% of pancreatic cancers arise, respectively?

Answer 92

15% in the body and 5% in the tail.

Question 93

What percentage of pancreatic cancers involve the entire pancreas?

Answer 93

In 20% of cases.

Question 94

What are the two characteristic features of pancreatic cancers regarding invasiveness and stromal reaction?

Answer 94

(1) Highly invasive, often extending into peripancreatic tissues; (2) Elicit an intense desmoplastic response.

Question 95

What does the intense desmoplastic response in pancreatic cancer lead to morphologically?

Answer 95

Deposition of dense collagen, making the tumor hard.

Question 96

Describe the typical macroscopic appearance of most pancreatic cancers (texture, shape, color, definition).

Answer 96

Hard, stellate, gray-white, poorly defined masses.

Question 97

What is the appearance of the pancreatic cancer mass due to the desmoplastic response?

Answer 97

Hard, stellate, and gray-white.

Question 98

What is the vast majority histological type of pancreatic carcinoma?

Answer 98

Adenocarcinoma.

Question 99

Microscopically, what kind of stroma is typically associated with pancreatic adenocarcinoma?

Answer 99

A dense desmoplastic (fibrotic) stroma.

Question 100

What pattern of growth do pancreatic adenocarcinomas typically show microscopically?

Answer 100

Glandular or ductal differentiation, often with irregular and infiltrating glands.