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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
Describe the activation of target cell receptor by insulin?
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
Grey Turner's sign
Extensive flank bruising in acute pancreatitis.
27
Investigations for acute pancreatitis?
Serum lipase concentrations - elevated! lasts longer than amylase Liver function - liver enzymes like transferase
28
Management of acute pancreatitis?
- Parenteral fluid replacement - analgesia - IV fluid replacement - antibiotics
29
Why is morphine avoided in the management of acute pancreatitis?
Morphine associated with contraction of sphincter of Oddi.
30
Investigation of chronic pancreatitis?
Serum amylase, may be increased during episodes of pain. Steatorrhoea - fat malabsorption
31
Pancreatic ascites
Persistent accumulation of massive amount of intraperitoneal fluid during course of chronic pancreatitis. Has high amylase content, high protein content
32
Describe factors which may result in pancreatic tumours?
- smoking (raises serum lipids) - increased fat - obesity - family history - chronic pancreatitis
33
Physical findings in a patient with pancreatic tumour
- Bile salt induced pruritus (itching) - palpable enlarged gall bladder - abdominal distention - ascites
34
Investigation of pancreatic tumour
Specific serum tumour markers | - carbohydrate antigen 19-9 (CA 19-9) and carcinoembryonic antigen (CEA) may be elevated in pancreatic cancer
35
Define acute pancreatitis?
Characterised by reversible pancreatic parenchymal injury associated with inflammation. - alcohol exposure - pancreatic duct exposure - vascular injury
36
Describe primary acinar cell injury? e.g. due to oxidative stress
May generate free radicals in acinar cells. Leading to membrane oxidation. Activation of transcription factors.
37
Effect of calcium on trypsin
If calcium concentration decreases then trypsin tends to cleave and inactivate itself
38
Hereditary pancreatitis could be caused by mutation in which gene?
SPINK1 | - gene encoding a trypsin inhibitor
39
Pain felt by patient, indicative of acute pancreatitis
Epigastric region. Radiating from mid back Sudden, constant and profound
40
Treatment of acute pancreatitis
IV crystalloid - subset of IV fluids. Fluid resuscitation in presence of hypovolemia, haemorrhage, sepsis and dehydration. - e.g. Ringer's lactate
41
Pathogenesis of pancreatitis
Bio acids, fatty acids can also induce increased release of calcium. Calcium can be toxic to cell function and cause necrosis.
42
Drug development for acute pancreatitis
Calcium entry inhibition targeting orai calcium channels. Orai channels - activated upon the depletion of internal calcium stores.
43
Aetiology of chronic pancreatitis
``` Alcohol Smoking Metabolism Hereditary Obstruction Autoimmune Neoplasm ```
44
Diagnosis of chronic pancreatitis
- Chronic upper abdominal / mid back pain that may be intermittent or continuous. - Steatorrhoea (greasy floating stools) - increased bone fractures - malnutrition
45
State some complications of chronic pancreatitis
``` Psuedocysts Pancreatic fistulae Biliary obstruction Duodenal obstruction Portal hypertension Malnutrition Carcinoma ```
46
Psuedocysts
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
Antimetic's
Drug which is effective against vomiting and nausea
48
Treatment of chronic pancreatitis
Pancreatic enzyme replacement therapy. Manage bone health progress with DEXA scan. Management of pain with pharma, surgical intervention.
49
Describe pancreatic enzyme replacement therapy
Enzymes: granules, tablets, enteric coated, mini-microspheres, non-coated FDA approved: creon, pancreaze, pertzye, ultrase, viokase and zen pep.
50
Presentation of pancreatic cancer
- 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
Describe surgery for pancreatic cancer
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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