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MBChB221 Digestive > Pancreas Physiology > Flashcards

Pancreas Physiology Flashcards

1
Q

Pancreas Exocrine Cells name

A

Acinar
-> With zymogen granules (enzyme precursors)

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2
Q

Acute Pancreatitis cause

A

Injury to acinar cells -> autodigestion + immune inflammation
- Itself due to several causes: alcohol, gallstones main

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3
Q

Severity of acute pancreatitis

A

Spectrum: 30-40% cases are severe with 20-30% mortality (ie quite high)

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4
Q

Autodigestive Proteases cause

A

Destruction of pancreas acini

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5
Q

Autodigestive Lipases cause

A

Necrosis of fat in pancreas and other sites

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6
Q

Autodigestive elastases cause

A

Blood vessel destruction = internal haemorrhage

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7
Q

Why is acute pancreatitis so severe

A

Standard inflammatory response is compounded by activation of digestive enzymes leading to autodigestion

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8
Q

Clinical signs of acute pancreatitis

A

Epigastric pain
Nausea, vomiting, fever, abdominal tenderness

(Non specific)

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9
Q

How to diagnose acute pancreatitis

A

Initially neutrophil count to see if inflammation

Then to specify pancreatitis:
1 Elevated serum amylase and lipase
2 CT scan

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10
Q

How to manage acute pancreatitis

A

IV fluids

Nasogastric suction to remove the pancreatic enzymes

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11
Q

Chronic Pancreatisis presentation

A

Fibrotic due to repeated inflammation

Atrophy = smaller pancreas

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12
Q

Chronic Pancreatisis cause

A

Repeated inflammation of pancreas (often due to heavy alcohol intake)

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13
Q

Chronic Pancreatisis complications

A

Loss of exocrine function = malabsorption

If very severe spreads from acini to islets of langheran = endocrine complications (diabetes)

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14
Q

Pancreatic Carcinoma deaths

A

Very high despite actual cancer being uncommon (as high fatality due to late presentation)

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15
Q

Pancreatic cancer, what is the type of cancer

A

Adenocarcinoma as glandular tissue

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16
Q

Where are pancreatic carcinomas most common

A

Head of pancreas

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17
Q

Complications of head of pancreas cancer

A

Biliary obstruction

18
Q

Diagnosis of pancreatic cancer

A

Imaging (CT US) confirmed by biopsy

19
Q

Endocrine pancreatic tumour name

A

Insulinoma (Rare)

20
Q

Ductal cell of pancreas secretion

A

Bicarbonate

21
Q

Acinar cell secretion

A

Digestive enzymes

22
Q

Bicarbonate secretion steps

A
  1. HCO3- from blood into ductal cells, and HCO3- made in ductal cells from H2O and CO2
  2. Secreted via activate transport (CFTR and Cl-/HCO3- exchanger)
23
Q

How does secretin increase bicarbonate secretion from the pancreas

A

Secretin -> cAMP -> CFTR -> HCO3-

24
Q

How does vagal stimulation increase bicarbonate secretion from the pancreas

A

Vagal afferents -> Calcium -> increased HCO3- secretion

25
Q

Acinar cells high in which organelle

A

Endoplasmic reticulum to make lots of enzymes

26
Q

What mediates release of pancreatic enzymes

A

CCK

27
Q

How does CCK stimulate pancreatic enzyme secretion

A
  1. Hormone in blood -> acinar cells stimulated
  2. Activates vagus Efferents next to I cell -> brainstem -> vagus afferents stimulate acinar cells
28
Q

Trypsinogen -> trypsin enzyme

A

Enterokinase

29
Q

Trypsin cleaves which enzymes

A

Trypsinogen (auto catalytic)
Chymotrypsingen
Carboxypeptidase
+ others

30
Q

Protease

A

Enzyme that digests protein

31
Q

Lipase function

A

Triglycerides -> monoglycerides / free fatty acids

32
Q

Amylase function

A

Starch -> sugar

33
Q

What pre-empts the pancreas to begin releasing enzymes into the duodenum

A

Gastrin release during gastric phase of digestion

34
Q

Inhibitors of pancreatic enzyme secretion

A

Glucagon
Somatostatin
Pancreatic polypeptide
Peptide YY (from colon ie further down)

35
Q

What happens with Cystic Fibrosis disease

A

Defective CFTR -> thick mucus clogs things eg ducts

36
Q

Impact of defective CFTR on pancreatic secretion thickness

A

Inc Cl- accumulation in cells -> inc Na+ accumulation from lumen -> inc H2O absorbed from lumen

= Pancreatic secretions less water = thick (hyperviscous)

37
Q

Impact of defective CFTR on pancreatic enzymes in the pancreas

A

Accumulation of enzymes in the pancreas (as clogged duct from thick secretion) = autodigestion of pancreas = Pancreatisis

38
Q

Pancreas divisum

A

Failure of the pancreatic ducts to fuse = small flow as two ducts but one exit = blockage = Pancreatisis from autodigestion due to accumulation of enzymes

39
Q

Pancreatic insuffiency how much loss of exocrine function needed

A

> 90%

40
Q

Which enzyme is most critically lost during pancreatic insufficiency

A

Lipase = fat malabsorption

41
Q

Impacts of fat malabsorption (eg loss of lipase)

A

Weight loss

Steatorrhoea (fat in stool)

MBChB221 Digestive (9 decks)

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