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GI - Y2 > L13 - Pancreatitis & Pancreatic cancer > Flashcards

L13 - Pancreatitis & Pancreatic cancer Flashcards

1
Q

Pancreatitis

A

Inflammatory process, pancreatic enzymes auto digest gland

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2
Q

Briefly state function of endocrine and exocrine pancreas?

A

Endocrine: Insulin production

Exocrine: Digestive enzymes

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3
Q

Briefly describe enzyme production and travel?

A
  • Pancreatic acinar cell produce digestive enzymes.
  • Packaged in golgi to produce zymogens
  • zymogens travel to pancreatic ductal cell
  • pancreatic duct
  • small intestine
  • brush border of duodenum
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4
Q

Enzymes are stimulated by the release of?

A
  • vagal nerve
  • VIP
  • GRP (gastrin releasing peptide)
  • secretin
  • CCK
  • encephalins
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5
Q

How is Trypsinogen converted to active form?

A

Enterokinase will cleave the N-hydroxyterminal hexapeptide fragment from Trypsinogen to form trypsin.

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6
Q

What limits further pancreatic secretion?

A

Elevated levels of trypsin (unbound from digested food) lead to decreased CCK and secretin levels.

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7
Q

How is premature activation of pancreatic enzymes limited?

A
  • proteins translated into inactive pro enzymes

- pro-enzymes packaged in paracrystalline arrangement with protease inhibitor.

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8
Q

Common cause of biliary tract disease?

A

Gall stone in bile duct.

Getting temporarily lodged in sphincter of Oddi.

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9
Q

Describe how presence of alcohol may lead to blockage of pancreatic outflow?

A
  1. Ethanol lead to intracellular accumulation of digestive enzymes, premature activation & release
  2. Increases permeability of ductules
    - enzymes reach parenchyma
    - pancreatic damage
  3. Increases protein content of pancreatic juice
  4. Decreases HCO3- level
  5. Decreases trypsin inhibitor concentration

Leads to formation of protein plugs - blocks pancreatic outflow

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10
Q

Describe chronic pancreatitis?

A

Continuing, inflammatory process of the pancreas, characterised by irreversible morphological change.

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11
Q

Signs / symptoms of chronic pancreatitis?

A

Abdominal pain.
Intermittent attacks of severe pain, often in mid abdomen or left upper abdomen.
Diarrhoea.
Weight loss.

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12
Q

What might be seen on a CT of a patient with chronic pancreatitis?

A

Inflammation, calcium deposits.
Pancreatic calcification.
Dilated duct.

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13
Q

Describe endoscopic retrograde cholangiopancreatography?

A
  • Endoscopy and fluroscopy to visualise and treat problems of the biliary and pancreatic duct.
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14
Q

Compare and contrast acute and chronic pancreatitis?

A

Acute Pancreatitis

  • Severe abdo pain.
  • Nausea, vomitting.
  • Inflamed (neutrophil and oedema)
  • serum amylase and lipase HIGH
  • most patients make full recovery

Chronic pancreatitis

  • irreversible
  • inflammation (monocyte & lymphocyte)
  • leads to fibrosis and calcification
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15
Q

How may pancreatic fibrogenesis occur?

A
  1. (GF, cytokines, chemokines) leads to deposition of ECM & fibroblast proliferation
  2. Pancreatic injury: local expression and release of transforming growth factor beta
  3. TGF beta, stimulates growth of cells of mesenchymal origin
  4. Enhances synthesis of ECM proteins: collagen, fibronectin and proteoglycan
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16
Q

Describe alcoholic chronic pancreatitis?

A
  1. Alcohol increases acinar cell protein secretion
  2. Decreases fluid , HCO3- from ductal epithelial cells.
  3. Hence viscous fluid, results in proteinaceous debris coagulating in lumen
  4. Ductular obstruction
  5. Upstream acinar atrophy and fibrosis
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17
Q

Role of cytochrome P450?

A

Involved in formation and metabolism (breakdown) of various molecules and chemicals within cells.

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18
Q

Describe metabolism of alcohol?

A
  • Alcohol dehydrogenase oxidatively metabolises alcohol first to acetylaldehyde - acetate
  • If concentration of alcohol increases, cytochrome P450 2E1 induced to meet metabolic demands
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19
Q

Describe enzymes involved in protein synthesis?

A

Trypsin & Chymotrypsin - partially digested peptides to various sizes

Carboxypolypeptidase - some peptides split into amino acids

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20
Q

Describe basic stimuli causing pancreatic secretion

A

ACH
- released from parasymp vagus nerve ending and from other cholinergic nerves in enteric nervous system

CCK & secretin
- secreted by duodenal, jejunal mucosa when food enters small intestine

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21
Q

Describe the secretion of bicarbonate into lumen of duct?

A
  1. CO2 diffuses into cell from blood.
  2. CO2 + H20 —carbonic anhydrase— H+ + HCO3-
  3. Additional co-transport of HCO3- with Na+ from basolateral side
  4. HC03- exchanged for Cl- by secondary active transport through luminal border of cell to lumen of duct
  5. Cl- entering is recycled back to lumen via Cl- channel
  6. H+ exchanged for Na+ basolateral side
  7. Lumen, strong negative charge, pulls Na+ in across tight junctions
22
Q

Briefly describe phases of pancreatic secretion?

A
  1. Cephalic
    - ACH released by vagal nerve endings
    - enzymes secreted into pancreatic acini
  2. Gastric
    - nerve stimulation of enzyme secretion continues, accounting for more enzymes
  3. Intestinal
    - chyme enters small intestine
23
Q

CCK release via blood stream causes

A
  1. Gall bladder contraction

2. Relaxation of sphincter of Oddi

24
Q

Summarise Islet of Langerhan

A

A - glucagon
B - Insulin
D - Somatostatin
PP-cell - pancreatic polypeptide

25
Q

Describe the activation of target cell receptor by insulin?

A
  1. Insulin binds to alpha subunit of receptor
  2. autophosphorylation of the B-subunit receptor
  3. Induces tyrosine kinase activity
  4. Receptor tyrosine kinase activity begins a cascade of cell phosphorylation that increases or decreases the activity of enzymes.
26
Q

Grey Turner’s sign

A

Extensive flank bruising in acute pancreatitis.

27
Q

Investigations for acute pancreatitis?

A

Serum lipase concentrations
- elevated! lasts longer than amylase

Liver function
- liver enzymes like transferase

28
Q

Management of acute pancreatitis?

A
  • Parenteral fluid replacement
  • analgesia
  • IV fluid replacement
  • antibiotics
29
Q

Why is morphine avoided in the management of acute pancreatitis?

A

Morphine associated with contraction of sphincter of Oddi.

30
Q

Investigation of chronic pancreatitis?

A

Serum amylase, may be increased during episodes of pain.

Steatorrhoea
- fat malabsorption

31
Q

Pancreatic ascites

A

Persistent accumulation of massive amount of intraperitoneal fluid during course of chronic pancreatitis.
Has high amylase content, high protein content

32
Q

Describe factors which may result in pancreatic tumours?

A
  • smoking (raises serum lipids)
  • increased fat
  • obesity
  • family history
  • chronic pancreatitis
33
Q

Physical findings in a patient with pancreatic tumour

A
  • Bile salt induced pruritus (itching)
  • palpable enlarged gall bladder
  • abdominal distention
  • ascites
34
Q

Investigation of pancreatic tumour

A

Specific serum tumour markers

- carbohydrate antigen 19-9 (CA 19-9) and carcinoembryonic antigen (CEA) may be elevated in pancreatic cancer

35
Q

Define acute pancreatitis?

A

Characterised by reversible pancreatic parenchymal injury associated with inflammation.

  • alcohol exposure
  • pancreatic duct exposure
  • vascular injury
36
Q

Describe primary acinar cell injury?

e.g. due to oxidative stress

A

May generate free radicals in acinar cells.
Leading to membrane oxidation.
Activation of transcription factors.

37
Q

Effect of calcium on trypsin

A

If calcium concentration decreases then trypsin tends to cleave and inactivate itself

38
Q

Hereditary pancreatitis could be caused by mutation in which gene?

A

SPINK1

- gene encoding a trypsin inhibitor

39
Q

Pain felt by patient, indicative of acute pancreatitis

A

Epigastric region.
Radiating from mid back
Sudden, constant and profound

40
Q

Treatment of acute pancreatitis

A

IV crystalloid

  • subset of IV fluids. Fluid resuscitation in presence of hypovolemia, haemorrhage, sepsis and dehydration.
  • e.g. Ringer’s lactate
41
Q

Pathogenesis of pancreatitis

A

Bio acids, fatty acids can also induce increased release of calcium.
Calcium can be toxic to cell function and cause necrosis.

42
Q

Drug development for acute pancreatitis

A

Calcium entry inhibition targeting orai calcium channels.

Orai channels - activated upon the depletion of internal calcium stores.

43
Q

Aetiology of chronic pancreatitis

A 
Alcohol 
Smoking 
Metabolism 
Hereditary 
Obstruction 
Autoimmune 
Neoplasm
44
Q

Diagnosis of chronic pancreatitis

A
  • Chronic upper abdominal / mid back pain that may be intermittent or continuous.
  • Steatorrhoea (greasy floating stools)
  • increased bone fractures
  • malnutrition
45
Q

State some complications of chronic pancreatitis

A 
Psuedocysts 
Pancreatic fistulae 
Biliary obstruction 
Duodenal obstruction 
Portal hypertension 
Malnutrition 
Carcinoma
46
Q

Psuedocysts

A

Cysts but lack epithelial or endothelial cells.

An acute pancreatic pseudocyst is made up on pancreatic fluids with a wall of fibrous tissue or granulation.

47
Q

Antimetic’s

A

Drug which is effective against vomiting and nausea

48
Q

Treatment of chronic pancreatitis

A

Pancreatic enzyme replacement therapy.

Manage bone health progress with DEXA scan.

Management of pain with pharma, surgical intervention.

49
Q

Describe pancreatic enzyme replacement therapy

A

Enzymes: granules, tablets, enteric coated, mini-microspheres, non-coated

FDA approved: creon, pancreaze, pertzye, ultrase, viokase and zen pep.

50
Q

Presentation of pancreatic cancer

A
  • weakness / fatigue (86%)
  • loss of appetite (85%)
  • weight loss (85%)
  • abdominal pain (79%)
  • dark urine (59%)
  • jaundice (56%)
  • nausea (51%)
  • back pain (49%)
  • diarrhoea (44%)
  • vomiting (33%)
51
Q

Describe surgery for pancreatic cancer

A
  1. Pancreaticojejunostomy: pancreatic juice enters jejunum
  2. Hepaticojejunostomy: bile enters jejunum
  3. Duodenojejunostomy: restores continuity of GI tract, food passes to jejunum from stomach, preserving pylorus function.

GI - Y2 (18 decks)

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