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GIS > GIS25 Pathology Of The Pancreas > Flashcards

GIS25 Pathology Of The Pancreas Flashcards

1
Q

Anatomy of pancreas

A
  • Secondarily Retroperitoneal organ
  • 85-90g
  • 3 parts: head, body, tail
  • main pancreatic duct connect with common bile duct at Ampulla of Vater and drain into duodenum
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2
Q

Normal histology of pancreas

A

Exocrine: secretes digestive enzymes
- Acinar cells
- enzymes breakdown carbohydrates, proteins, fats and acids in duodenum
- enzymes go along pancreatic duct inactive until entering duodenum where they are activated
—> α-Amylase
—> Proteolytic peptidases (Trypsin, Chymotrypsin)
—> Lipase
—> Nuclease

Endocrine: islets of Langerhans: secretes hormones

  • β cell (insulin)
  • α cell (glucagon)
  • δ cell (somatostatin)
  • pp cell (pancreatic polypeptide)
  • hormones travel through blood to target organs
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3
Q

Pathologies in pancreas

A
  1. Congenital anomalies
  2. Cysts
  3. Pancreatitis
  4. Tumours
    - endocrine component
    - exocrine component
    - others (haematolymphoid, mesenchymal, metastasis)
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4
Q

Congenital anomalies

A
  1. Agenesis (very rare)
  2. Pancreas divisum (3-10%)
    - predisposes to chronic pancreatitis
    - drain into small intestine directly instead of draining into bile duct first —> minor duodenal papilla —> smaller opening —> ***predispose to inflammation
  3. Ectopic pancreas (pancreatic tissue grown outside its normal location and without vascular or other anatomical connections to the pancreas)
    - stomach, duodenum, jejunum, Meckel’s diverticulum, ileum
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5
Q

Pancreatitis

A
  • self-limiting to life-threatening
  • Acute pancreatitis: reversible with insult removed
  • Chronic pancreatitis: progressive / irreversible destruction of exocrine pancreas due to repeated attacks of focal and mild inflammation and necrosis (loss of pancreas parenchyma) —> replaced by ***fibrosis
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6
Q

Acute pancreatitis etiologies

A
  • ***Biliary tract disease
  • ***Alcoholism
  • Obstruction of pancreatic duct
  • Medications
  • Infections e.g. mumps, coxsackie virus
  • Trauma
  • Metabolic disorder e.g. hypertriglyceridemia
  • Idiopathic / genetic
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7
Q

***Acute pancreatitis pathogenesis

A

**Autodigestion of parenchyma by **inappropriately activated enzymes through 3 possible pathways:

1. ***Pancreatic duct obstruction
—> interstitial edema
—> ↓ bloodflow
—> ischaemia
—> ***acinar cell injury
—> activated enzymes
  1. Primary ***acinar cell injury
    —> release of Intracellular proenzyme and lysosomal hydrolase
    —> activation of enzyme
  2. Defective **intracellular transport of proenzymes within acinar cells
    —> delivery of proenzyme to lysosomal compartment
    —> **    intracellular activation of enzyme

ALL lead to

  1. Inflammation, edema
  2. Proteolysis
  3. Fat necrosis
  4. Haemorrhage
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8
Q

***Acute pancreatitis clinical features

A
  1. **Sudden onset of abdominal pain and vomiting some time (1-2 hours) **after meal
  2. Associated ***shock, acute renal failure and adult respiratory distress syndrome
  3. Raised serum ***amylase level
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9
Q

Acute pancreatitis morphology

A
  1. Necrosis of pancreatic tissue (blurred cell contour)
  2. Haemorrhage due to damage of vasculature
  3. Yellow chalky fat necrosis

(1. Inflammation, edema
2. Proteolysis
3. Fat necrosis
4. Haemorrhage)

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10
Q

Acute pancreatitis complications

A
  1. Systemic organ failure (shock)
  2. Chemical ***peritonitis
  3. Retroperitoneal ***haemorrhage
  4. Local abscess
  5. ***Pseudocyst formation (cyst without normal epithelial lining)
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11
Q

Chronic pancreatitis etiology

A

Similar to acute pancreatitis, with Chronic alcoholism > Biliary tract diseases

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12
Q

***Chronic pancreatitis pathogenesis

A
  1. Ductal obstruction by ***concretions
  2. ***Toxic-metabolic events
  3. ***Oxidative stress
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13
Q

Chronic pancreatitis clinical features

A
  1. Bouts of abdominal pain, precipitated by alcohol intake / overeating
  2. **Pancreatic insufficiency
    - **    malabsorption
    - **weight loss
    - **    steatorrhoea
    - hypoalbuminemia
    - ***diabetes mellitus
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14
Q

Macroscopic and microscopic features of chronic pancreatitis

A

Macroscopic:

  • **Fibrotic parenchyma with focal cystic change due to ductal **dilatation
  • Stones occasionally seen inside pancreatic ducts

Microscopic:

  • Irregular acinar **atrophy and **periductal fibrosis with relative preservation of islets
  • Chronic ***inflammatory infiltrates around lobules and ducts
  • Some ducts show ***ectasia (dilatation)
  • **Rmb:
    1. Fibrosis
    2. Ductal dilatation
    3. Chronic inflammatory cell infiltration
    4. Acinar atrophy
    5. Stones
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15
Q

Chronic pancreatitis complications

A
  1. Pseudocyst
  2. Duct obstruction
  3. Malabsorption
  4. Steatorrhoea
  5. Secondary diabetes
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16
Q

Pancreatic cysts

A
  1. **Pseudocyst
    - 75% of pancreatic cysts
    - result of acute / chronic pancreatitis
    - NO epithelial lining, with localised collection of **    necrotic-haemorrhagic material
  2. Congenital
    - polycystic disease
  3. Other cysts
    - lymphoepithelial cyst, parasitic cyst, endometriotic cyst
  4. Cystic neoplasms
    - only 5-15% pancreatic cysts are neoplastic
    - Serous cystadenomas (almost always benign)
    - Mucinous cystic neoplasms (benign/borderline/malignant)
    - Intraductal papillary mucinous neoplasms (benign/borderline/malignant)
17
Q

Pancreatic adenocarcinoma

A
  • ***Adenocarcinoma: commonest histological subtype of pancreatic carcinoma
  • arise from ***Ductal epithelium
  • ***high mortality rate, 5-year survival rate <5%
  • head (60%), body (15%), tail (5%), diffuse (20%)

Carcinogenesis:
- progresses from benign to malignant through precursor lesions called ***Pancreatic intraepithelial neoplasias (PanINs)

Risk factors:

  • smoking
  • chronic pancreatitis and diabetes

Biological behaviour:

  • metastases to regional lymph nodes, liver, lung, peritoneum, omentum and adrenal glands
  • paraneoplastic manifestations: migratory thrombophlebitis, peripheral neuropathy
18
Q

Pancreatic adenocarcinoma clinical features

A
  1. Presents late (esp. body and tail)
  2. Pain
  3. ***Obstructive jaundice (head) (early presentation: better prognosis)
  4. Weight loss, malaise, anorexia
  5. Migratory ***thrombophlebitis (inflammatory process: blood clot form and block veins) in 10% case
19
Q

Pancreatic adenocarcinoma microscopic features

A
  1. Arise from pancreatic duct
  2. Bizarre, ***Distorted glands with mucin production
  3. Wildly infiltrative with a ***fibrotic stroma
  4. Tumour cells showing marked ***nuclear anaplasia (poor cell differentiation) and frequent mitosis
  5. Prone to perineural invasion
20
Q

Pathologies of endocrine pancreas

A
  1. Diabetes mellitus
  2. Tumours
    - Islet cells tumours are rare (vs tumours of the exocrine pancreas)
    - commonly affect adults
    - hormonally functional / non-functional
  3. Insulinoma —> Hypoglycaemia
  4. Glucagonoma —> Secondary diabetes
  5. Gastrinoma —> Severe peptic ulcer (Zollinger-Ellison syndrome) (***G cells in pancreas secrete Gastrin)
  6. VIPoma (***vasoactive intestinal peptide) —> Water diarrhoea

GIS (29 decks)

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