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SYSTEMIC PATHOLOGY > Hepatobiliary - pancreas > Flashcards

Hepatobiliary - pancreas Flashcards

1
Q

congenital anomalies of pancreas

A
  • Pancreas divisum (most common)
  • Annular pancreas
  • Ectopic pancreas
  • Agenesis
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2
Q

pancreas divisum

A

a single pancreatic duct is not formed - remains as two distinct dorsal and ventral ducts

may cause chronic pancreatitis, but most remain asymptomatic

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3
Q

pancreas histology

- 2 types of cells + function

A
  • exocrine (secretion of hormones through ducts)
    acinar cells: produce proenzymes -> GIT (for gastric motility/ gastric acid secretion)
  • endocrine (w/p ducts)
    islets of langerhans produce: insulin, glucagon, somatostatin
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4
Q

pancreatitis

- pathogenesis

A

injuries leading to autodigestion of the pancreas by its own digestive enzymes
(activated by trypsin)

trypsin activity need to be inhibited by acinar and ductal cells so it wont activate the proenzymes IN the pancreas -> wont get autodigested

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5
Q

acute pancreatitis

- risk factors/ causes

A

Reversible pancreatic parenchymal injury associated with inflammation

I GET SMASHED
- Idiopathic
- Gallstone (F>M)
- Ethanol (M>F)
- Trauma
- Steroids
- Mumps and other infections
- Autoimmune – SLE, PAN
- Scorpion toxin 
- Hypercalcemia, hypertriglyceridemia, 
hypothermia
- ERCP (endoscopic retrograde cholangiopancreatography - used to diagnose pancreatic diseases - may cause trauma to pancreas)
Drugs (furosemide, azathioprine)
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6
Q

acute pancreatitis

pathogenesis

A

caused by inappropriate release and activation of pancreatic enzymes

  • > destroy pancreatic tissue
  • > elicits acute inflammatiom
  • ductal obstruction: increase intrapancreatic ductal pressure -> accumulation of enzyme rich fluid in pancreatic interstitium
  • acinar cell injury
  • defective intracellular transport
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7
Q

alcohol causing acute pancreatitis

A
  • increase in contraction of sphincter of Oddi (SM of bile duct)
  • causes secretion of protein-rich pancreatic fluid -> deposition of inspissated protein plugs and obstruction of small pancreatic ducts
  • Direct toxic effects on acinar cells -> oxidative stress
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8
Q

acute pancreatitis clinical presentation and diagnosis

A
  • Constant intense abdominal pain (may be referred to upper back or left shoulder)
  • nausea, vomiting and loss of appetite
  • SIRS (systemic inflammatory response: caused by release of toxic enzymes, cytokines and other mediators into the circulation

diagnosis:
↑ serum amylase (1st 24 hrs) & lipase (72-96 hrs)

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9
Q

acute pancreatitis

- gross (2) and histo (5) features

A
  • hemorrhage and necrosis at head of pancreas
  • presence of omental fat (visceral fat in omentum - btw the organs)
  • microvascular leak and oedema
  • fat necrosis
  • acute inflammation
  • destruction of pancreatic parenchyma
  • destruction of blood vessels and interstitial
    hemorrhage
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10
Q

acute pancreatitis

complications

A

Systemic organ failure

  • Shock (due to systemic inflammatory response syndrome)
  • Acute respiratory distress syndrome (ARDS)
  • Acute renal failure (acute renal tubular necrosis)
  • Disseminated intravascular coagulation
  • formation of pancreatic pseudocyst (collection of necrotic and haemorrhagic material rich in pancreatic enzymes - benign cyst)
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11
Q

chronic pancreatitis

  • definition
  • who it affects
A

Prolonged inflammation of the pancreas associated with irreversible destruction of exocrine/ endocrine (late stage) parenchyma

middle-aged males

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12
Q

pathogenesis of chronic pancreatitis

A

after many recurrences of acute pancreatitis

fibrogenic factors (TGF-ß, PDGF) induce activation and proliferation of myofibroblasts -> collagen deposition and fibroblasts

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13
Q

chronic pancreatitis

  • clinical presentation
  • diagnosis
A

repeated and persistent episodes of abdominal pain
worse w/ alcohol/ overeating/ drugs (opiates) -> increase sphincter of Oddi tone (stimulate the contraction)

diagnosis:
CT scan/ ultrasound - pancreatic calcifications

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14
Q

chronic pancreatitis

- complications

A
  • Pancreatic exocrine insufficiency
  • > Chronic malabsorption
  • Endocrine insufficiency -> Diabetes mellitus (cause of decrease insulin)
  • Severe chronic pain
  • formation of pancreatic pseudocysts
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15
Q

chronic pancreatitis

- histo features

A
  • dilatation of pancreatic ducts with protein plugs/ calcified concretions
  • Fibrosis
  • Atrophy and dropout of acini, with relative sparing of islets
  • Pseudocysts
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16
Q

non-neoplastic pancreatic masses

A
  • pseudocysts
  • congenital cysts

solid mass:
- AI (autoimmune) pancreatitis

17
Q

cystic neoplastic pancreatic masses

A
  • Serous cystadenoma (benign)

pre-malignant

  • intraductal papillary mucinous neoplasm (IPMN)
  • mucinous cystic neoplasm (MCN)

malignant lesions is just pre-malignant becoming invasive

18
Q

solid neoplastic pancreatic masses

A
  • ductal adenocarcinoma
  • acinar cell carcinoma
  • pancreatoblastoma
  • neuroendocrine tumour (panNET)
19
Q

diagnostic method for pancreatic masses

A
  • Endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) cytology
  • cyst fluid analysis (amylase levels, KRAS mutation)
20
Q

pseudocysts complications

A

pseudocyst = collection of necrotic and haemorrhagic material rich in pancreatic enzymes. does not have epithelial lining

complications:
Spontaneously resolves, secondary infection or compress / perforate adjacent structures

21
Q

congenital cysts

- gross and micro appearance

A
  • Unilocular, thin-walled, containing serous fluid

- Thin fibrous wall lined by single layer of variably attenuated uniform cuboidal epithelium

22
Q

(infiltrative) ductal carcinoma
- who does it affect + risk factors
- prognosis

A
  • 60-80 yrs
  • Smoking, high-fat diet, chronic pancreatitis, DM, genetic predisposition (BRCA2, CDKN2A)

high mortality cause of aggressiveness

23
Q

(infiltrative) ductal carcinoma pathogenesis

A

gene mutation -> invasive
[KRAS, CDKN2A, TP53 and
SMAD4 = tumour suppressors]
(basically affect the normal production of the tumour suppressors = uncontrolled cell growth -> carcinoma)

KRAS: affect tyrosine kinase activity - affects cell growth and survival

CDKN2A: cyclin dependent kinase inhibitor

SMAD4: signal transduction

TP53:

  1. arresting cell growth
  2. inducing cell death
  3. causing cellular senescence
24
Q

(infiltrative) ductal carcinoma

- clinical presentation

A
  • may be asymptomatic
  • Pain
  • Obstructive jaundice (HOP lesions)
  • Systemic symptoms (advanced disease – LOW, LOA??, lethargy)
  • Trosseau sign: platelet-activating factors and procoagulants from tumour or its necrotic products
25
Q

(infiltrative) ductal carcinoma

- diagnosis

A

serum carcinoembryonic antigen (CEA) levels
imaging
core biopsy

26
Q

neuroendocrine tumour (panNET)

  • histo features
  • diagnostic findings
A
  • Solid pale masses
  • cystic change
  • islands and trabeculae of small round cells with ‘salt and pepper’ chromatin
  • Highly vascular
  • Immunohistochemical stain for neuroendocrine and secretory products
  • Ultrastructural image of neurosecretory granules in cytoplasm

SYSTEMIC PATHOLOGY (27 decks)

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