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Cell Path > Endocrine 1 - Exocrine Pancreas > Flashcards

Endocrine 1 - Exocrine Pancreas Flashcards

1
Q

What 4 components comprise the pancreas?

A

Head, neck, body, tail

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2
Q

What % of the pancreas does the exocrine component comprise?

A

80-85%

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3
Q
  1. The main pancreatic duct comprises the:

2. What is another important duct?

A
  1. Hepatopancreatic duct (Ampulla of Vater) and hepatopancreatic sphincter (Sphincter of Oddi)
  2. Accessory pancreatic duct (abnormalities during development can result in this duct acting as the main duct)
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4
Q

What are the 2 main functional units of the exocrine pancreas?

A
  1. Acinar cells

2. Ductal structures

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5
Q

What do the ACINAR, CENTRO-ACINAR & COLUMNAR CELLS each secrete?

A

A: proenzymes (which are digestive enzymes)
C-A: neutralise pH by secreting bicarbonate ions
C: produce mucin which acts as a chemical barrier

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6
Q

How are proenzymes activated?

A

By ENTEROPEPTIDASE in chyme in the upper duodenum. This converts trypsinogen to trypsin which then initiates a cascade in which trypsin activates the other 5 enzymes. Therefore abnormal activation of trypsin = bad

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7
Q

Which 6 digestive enzymes comprise the PANCREATIC JUICE? What do they each break down?

A
  1. Trypsinogen – breaks down protein (trypsin = the active form)
  2. Chymotrypsinogen - breaks down protein
  3. Procarboxypeptidase – breaks down protein
  4. Proelastase – breaks down elastin and collagen
  5. Kallikreinogen - cleave kininogens to form kinins
  6. Prophospholipase A and B – hydrolises lipids
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8
Q

What does SPHINK1 code for?

A

Trypsin inactivators - your bodies defence for when trypsin is activated at the wrong time

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9
Q

What 2 things does secretion of cholecystokinin (CCK) from the duodenum do?

A
  1. Stimulates the release of the digestive enzymes from the pancreas
  2. Stimulates the release of bile from the gall bladder
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10
Q

What does the PDX1 gene do?

A

Gene present during development involved in the formation of the pancreas.

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11
Q

What are 4 congenital abnormalities of the pancreas?

A
  1. Pancreas Divisum: duct systems fail to fuse, accessory duct acts as main duct
  2. Pancreatic agenesis: mutations of PDX1 gene during developement —> foetus dies
  3. Ectopic Pancreas: stomach, duodenum
  4. Annular Pancreas: forms as a ring-shape around duodenum instead of a nice, elongated gland
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12
Q

What is PANCREATITIS? What are its 2 subcategories?

A
  • Inflammation and activation of digestive enzymes in pancreas (they should only be activated in the duodenum)
  • Acute or Chronic (based on length of inflammation)
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13
Q

The body has 4 mechanisms it uses to protect itself when abnormal changes occur in the pancreas. What are these?

A
  • Maintenance of a zymogen granule
  • Secretion of a proenzyme (inactive) rather than an active enzyme
  • The pH conditions which are maintained by the bicarbonate ions
  • The chemical barrier formed by mucin
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14
Q

Is acute pancreatitis reversible?

A

Yes. Restoration of acinar cell mass occurs.

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15
Q

______ and _______ account for 80% of acute pancreatitis cases.
What are 5 other causes?

A
  • Alcoholism and Biliary tract disease
  • Metabolic (hypercalcemia), genetic (PRSS1 or SPINK1), mechanical (trauma), infectious (mumps), vascular (shock)
  • ** All of these cause ACINAR CELL INJURY which is ultimately what causes AP
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16
Q

What are 3 symptoms people with AP present with?

A
  1. Acute abdominal pain (URQ)
  2. Referred pain to upper back and left shoulder
  3. Nausea/vomiting
17
Q

What are 4 measurements used to diagnose AP?

A
  1. Abdominal distention + tenderness
  2. Increased WBC count
  3. Increased [serum] of pancreatic lipase + pancreatic amylase
  4. Fluid exudate as seen in CT scan
18
Q

Name 5 morphological changes seen in the pancreas of a person with AP.

A
  1. Destruction of pancreas parenchyma
  2. Oedema
  3. Chalky white fat appearance + necrosis
  4. Enlarged
  5. Interstitial haemorrhage
    * ** Reasons why are on Slide 7
19
Q

What 3 enzymes are inappropriately activated in AP?

A
  1. Trypsin: breakdown of proteins + activation of other pancreatic enzymes
  2. Phospholipase: breakdown of fat cells
  3. Elastase: breakdown of elastic fibres & vasculature
20
Q

Local inflammation is mediated by the release of PRO-INFLAMMATORY CYTOKINES. Which 4 in particular are released?

A

TNF-alpha
IL-1beta
IL-6
IL-8

21
Q

If not treated, AP can progress to what syndrome?

A

Systemic Inflammatory Response Syndrome (SIRS)

22
Q

What 5 things are done as treatment for AP?

A
  1. Fluid resuscitation to correct fluid loss
  2. Pain relief
  3. Nil by mouth to rest exocrine function
  4. Antiemetics for nausea + vomiting
  5. Drainage of fluids to relieve pressure
23
Q

Why are serum concentrations of amylase and pancreatic lipase not elevated in Chronic Pancreatitis?

A

Necrosis occurs in CP. The cells have gone past just apoptosis and are no longer able to perform any function anymore.

24
Q

What are 6 measurements used to diagnose CP?

A
  1. Abdominal distention + tenderness
  2. No change in serum amylase and lipase
  3. Potential for elevated BGLs and CCK
  4. Pancreatic calcifications observed using CT scan
  5. ERCP (endoscopy) to look for pancreatic + bile duct deformities
  6. Staining of faecal samples to test for steatorhhoea
25
Q

Name 3 morphological changes seen in the pancreas of a person with CP.

A
  1. Parenchymal fibrosis - reduced number and size of acini cells
  2. Inter + intra-lobular ducts have protein plugs
  3. Inflammatory infiltrate found in ducts with atrophic epithelium
26
Q

What are the 5 suggested causes of CP?

A
  1. Ductal theory (physical clogs and stuff)
  2. Acinar theory (more about chemicals/molecules/enzymes that damage the acinar cells)
  3. Two-hit theory
  4. Multiple cause theory (ischemia)
  5. Electrophilic stress (toxic – too much, deficiency – too little of something)
27
Q

______ is a key sign of AP

______ is a key sign of CP

A

Inflammation

Fibrosis

28
Q

What 4 steps occur in CP which lead to FIBROSIS occuring?

A
  1. Infiltrate and activation of macrophages
  2. Increased collagen synthesis, decreased collagen degradation
  3. Release of pro-fibrotic cytokines (TGbeta, PDGF)
  4. Release of pro-inflammatory cytokines (TNF-alpha)
29
Q

What 6 things are done as treatment for AP?

A
  1. Pain management
  2. Steroids
  3. Enzyme therapy (block CCK)
  4. Micronutrients (to combat Reactive Oxygen Species)
  5. Treatment of protein-energy malnutrition
  6. Surgery: lateral pancreaticojejunostomy (Puestow procedure)

Cell Path (29 decks)

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