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Pathology > Exocrine pancreas > Flashcards

Exocrine pancreas Flashcards

1
Q

Band-like ring of normal pancreatic tissue that completely encircles the 2nd portion of
duodenum

A

Annular pancreas

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2
Q

What is annular pnacreas ass w?

A

Congenital abnormalities

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3
Q

Presentation of annular pancreas

A

Early in life or in adults, with signs and symptoms of duodenal obstruction, such as gastric distention and vomiting

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4
Q

What is the most common congenital anomaly of the pancreas?

A

Pancreas divisum

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5
Q

Cause of Pancreas divisum

A

Failure of fusion of the fetal duct systems of the dorsal & ventral pancreatic primordium

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6
Q

What are the favoured sites of ectopic pancreas?

A

Mainly stomach and duodenum, but also in jejunum, Meckel diverticula, & ileum

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7
Q

Histological presentation of ectopic pancreas?

A

Localised in the submucosa; Normal-appearing pancreatic acini, glands, & sometimes islets of Langerhans

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8
Q

Clinical presentation of ectopic pancreas?

A

Pain, due to localised inflammation
Mucosal bleeding (rarely)
Islet cell neoplasm (approx. 2% of all cases)

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9
Q

Reversible pancreatic parenchymal injury, associated with inflammation

A

Acute pancreatitis

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10
Q

Cause of Acute pancreatitis

A

Biliary tract disease & alcoholism

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11
Q

What is the epidemiology of Acute Pancreatitis?

A

Gallstones present in 35-60% of cases.
About 5% of patients with gallstones develop pancreatitis.
Gender ratios: M:F = 1:3 (biliary tract disease) and M:F = 6:1 (alcoholism).

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12
Q

What are the main aetiologic factors of Acute Pancreatitis?(5)

A

Metabolic: Alcoholism, hyper-lipoproteinaemia, hypercalcaemia, drugs (e.g., azathioprine).
Genetic: Mutations in PRSS1 (cationic trypsinogen) and SPINK1 (trypsin inhibitor) genes.
Mechanical: Gallstones, trauma, iatrogenic injury.
Vascular: Shock, atheroembolism, vasculitis.
Infectious: Mumps.

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13
Q

What are the forms and morphology of Acute Pancreatitis?

A

Mild (Acute Interstitial Pancreatitis):

Mild inflammation, interstitial edema, and focal fat necrosis.
Fatty acids combine with calcium → Insoluble salts → Blue granular appearance.
Severe (Acute Necrotising Pancreatitis):

Necrosis of acinar, ductal tissues, and islets of Langerhans.
Vascular injury leads to intraparenchymal hemorrhages.

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14
Q

Describe the macroscopic features of Acute Pancreatitis.

A

Pancreatic parenchyma: Red-black hemorrhage with yellow-white fat necrosis.
Extra-pancreatic fat: Necrosis in omentum, mesentery, and even subcutaneous fat.
Peritoneal cavity: Serous, turbid fluid with fat globules.
Hemorrhagic pancreatitis: Extensive necrosis with marked hemorrhage.

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15
Q

What is the primary pathogenesis of Acute Pancreatitis?

A

Autodigestion by activated pancreatic enzymes.
Inappropriate activation of trypsin → Activates other pro-enzymes (e.g., phospholipase, elastase).
Leads to fat degradation, vascular damage, inflammation, and small-vessel thrombosis.

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16
Q

What are the mechanisms behind pancreatic enzyme activation?

A

1.Pancreatic duct obstruction:

Gallstones or sludge → Increased ductal pressure → Enzyme-rich fluid accumulation.
Fat necrosis and local inflammation → Vascular insufficiency.
2.Acinar cell injury:

Causes: Viruses (e.g., mumps), drugs, trauma.
3.Defective intracellular transport of pro-enzymes.

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17
Q

How does alcohol contribute to Pancreatitis?

A

Protein-rich pancreatic fluid → Ductal obstruction.
Increased exocrine secretion and sphincter of Oddi contraction.
Direct toxic effects on acinar cells.

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18
Q

What are the clinical features of Acute Pancreatitis?

A

Intense abdominal pain, radiating to the upper back or left shoulder.
Anorexia, nausea, and vomiting.
Laboratory findings: Elevated serum amylase (24h) and lipase (72–96h).

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19
Q

How is Acute Pancreatitis managed?

A

Total restriction of oral intake.
Supportive therapy: IV fluids and analgesia.

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20
Q

What are the complications of Acute Pancreatitis?

A

Acute Respiratory Distress Syndrome (ARDS) and Acute Renal Failure.
Sterile pancreatic abscess or pseudocyst (40-60% of cases).
Sequelae of Acute Necrotising Pancreatitis.

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21
Q

What causes of hereditary pancreatitis?

A

Most cases, germ-line (inherited) mutations in the cationic trypsinogen (PRSS1)

22
Q

Pathogenesis of hereditary pancreatitis?

A

Mutation in the PRSS1 gene → Resistance of Trypsin to cleavage by another trypsin molecule; Inappropriate activation of a small amount of this trypsin in the
pancreas → Activation of other digestive pro-enzymes → Development of pancreatitis

23
Q

Cause/Pathogenesis of hereditary pancreatitis

A
  • SPINK1 gene codes for a pancreatic secretory trypsin inhibitor Inhibition of trypsin
    activity, thus prevention of auto-digestion of the pancreas by activated trypsin
  • Inherited inactivating mutations in the SPINK1 gene → Development of Pancreatitis
  • Autosomal recessive mode of inheritance
24
Q

What is the pathogenesis of Chronic Pancreatitis?

A

Repeated episodes of Acute Pancreatitis lead to Chronic Pancreatitis.
Ductal obstruction by concretions: Increased protein concentrations → Formation of ductal plugs → Calcification → Formation of calculi → Obstruction of ducts.
Toxic effects: Alcohol and its metabolites directly damage acinar cells.
Oxidative stress: Alcohol-induced free radicals → Membrane lipid oxidation, activation of transcription factors (AP1, NF-κB) → Inflammation, fibrosis, and necrosis of acinar cells.
Gene mutations: Inappropriate activation of pancreatic enzymes.

25
Q

What are the macroscopic features of Chronic Pancreatitis?

A

Hard gland with dilated ducts and calcific concretions.

26
Q

What are the microscopic findings in Chronic Pancreatitis?

A

Parenchymal fibrosis.
Reduced number and size of acini, with relative sparing of the islets of Langerhans.
Dilation of pancreatic ducts: Intra-lobular and inter-lobular ducts with protein plugs.
Chronic inflammatory cell infiltrates around lobules and ducts.
Ductal epithelium: Atrophic, hyperplastic, or squamous metaplasia.

27
Q

How does oxidative stress contribute to Chronic Pancreatitis?

A

Alcohol-induced oxidative stress generates free radicals in acinar cells.
Leads to membrane lipid oxidation, activation of transcription factors (AP1, NF-κB), and the expression of chemokines, which attract mononuclear cells, contributing to inflammation, fibrosis, and acinar cell necrosis.

28
Q

What is the role of ductal obstruction in the development of Chronic Pancreatitis?

A

Increased protein concentrations in pancreatic juice lead to formation of ductal plugs.
These plugs calcify, forming calculi, which obstruct the pancreatic ducts, contributing to chronic inflammation and fibrosis.

29
Q

What happens to the pancreatic tissue in Chronic Pancreatitis?

A

The acinar cells decrease in number and size.
Fibrosis replaces normal pancreatic tissue.
Ducts become dilated and may contain protein plugs.

30
Q

Clinical features of chronic pancreatitis

A

Variable presentations/manifestations: Repeated attacks of moderately severe abdominal pain
Recurrent attacks of mild pain
Persistent abdominal and back pain
Entirely silent disease, until development of pancreatic insufficiency and Diabetes Mellitus
Other instances, recurrent attacks of jaundice or vague attacks of indigestion (dyspepsia)

31
Q

Diagnosis of chronic pancreatitis

A
  • CT & US: Visualisation of calcifications within the pancreas
  • Weight loss and hypo-albuminaemic oedema from malabsorption
31
Q

Progression of chronic pancreatitis

A

20-25 year mortality rate of 50%

31
Q

Complications of chronic pancreatitis

A
  • Development of severe pancreatic exocrine insufficiency and chronic malabsorption, as well as Diabetes Mellitus
  • Pancreatic pseudocysts, in about 10% of patients
  • Hereditary Pancreatitis (secondary to PRSS1 mutations) 40%-55% lifetime risk of Pancreatic Cancer development
31
Q

Result of anomalous development of the pancreatic ducts

A

Congenital cysts

31
Q

Macroscopic features of congenital cysts

A

Usually uni-locular, with thinwalled capsule and clear serous fluid;
Size: Up to 5 cm in diameter

32
Q

Localised collections of necrotic-haemorrhagic material, rich in pancreatic enzymes

A

Psedocsyts

32
Q

Causes of pseudocysts

A
  • After an episode of Acute Pancreatitis, often in the setting of Chronic Alcoholic
    Pancreatitis
  • Traumatic injury to the pancreas
32
Q

Congenital cysts representation

A

Congenital cysts may be sporadic, or part of autosomaldominant polycystic kidney disease
& von Hippel-Lindau disease (vascular neoplasms of the retina & cerebellum/brain-stem, together with congenital cysts [and neoplasms] in the pancreas, liver, and kidney)

32
Q

Localisation of pancreatic cancer

A

Approx. 60% Head of the pancreas
- 15% Body of the gland
- 5% T ail of the gland
- 20% Diffuse involvement of the entire gland

32
Q

Localisation of pseudocysts

A

i. Intra-pancreatic, ii. Within lesser omental sac, iii. In the retro-peritoneum or iv.
Sub-diaphragmatic

32
Q

Morphology of pseudocysts

A

Usually solitary
Central necrotic-haemorrhagic material, rich in pancreatic enzymes
Non-epithelial-lined fibrous walls of granulation tissue

32
Q

Epidemiology of pancreatic cancer

A

Fourth leading cause of cancer deaths in the US; Age: 60-80yrs

32
Q

Synonym of pancreatic cancer

A

Infiltrating Ductal Adeno-CA of Pancreas

32
Q

Progression of psedocysts

A
  • Spontaneous resolution
  • Secondary infection
  • Compression or perforation into adjacent structures (larger pseudocysts) Pseudocy
33
Q

Risk factors of pancreatic cancer

A
  • Cigarette smoking
  • Consumption of a diet rich in fats
  • Hereditary and Chronic Pancreatitis
  • Diabetes Mellitus
  • Familial clustering of Pancreatic Cancer (BRCA2 mutations [approx. 10% of cases] in
    Ashkenazi Jews; Mutations in CDKN2A [p16] in pancreatic CA Individuals from
    melanoma-prone families)
33
Q

Macroscopic features of pancreatic cancer

A
  • Hard consistency
  • Stellate structure
  • Gray-white color
  • Poorly defined mass
34
Q

Microscopic features of pancreatic cancer

A
  • No differences among the sites of localisation (head, body or tail)
  • Moderately to poorly differentiated Adeno-CA with poorly formed glands or cell
    clusters
  • Aggressive, deeply infiltrative growth pattern
  • Dense stromal fibrosis
  • T endency for peri-neural invasion
  • Lymphatic and large vessel invasion
    ✓ Less common variants of Pancreatic Cancer: i. AdenoSquamous Carcinomas, ii. Colloid
    Carcinoma, iii. Hepatoid Carcinoma, iv. Medullary Carcinoma, v. Signet-ring Cell CA
35
Q

Diagnosis of pancreatic cancer

A

Endoscopic ultrasonography and computed tomography

36
Q

Course of disease and prognosis of pancreatic cancer

A

Brief and progressive
✓ Prognosis: 5 year survival rate: Less than 5%

37
Q

Clinical Features of pancreatic cancer

A

“Silent” until invasion of the adjacent structures; Pain
Obstructive jaundice (cancer localised at the head of the pancreas)
Weight loss, anorexia, generalised malaise & weakness (signs of advanced disease)
Migratory thrombophlebitis (Trousseau sign) occurs in about 10% of patients

Pathology (26 decks)

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