WEEK 5 - Pancreatitis Flashcards

1
Q

Where is the pancreas located?

A

Located posterior to the stomach between the duodenum on the right and the spleen on the left

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2
Q

What are the four ANATOMICAL parts of the pancreas and where are they located?

A
  1. Head - tucked into the curve of the duodenum
  2. Neck - 2cm long, overlies the superior mesenteric artery
  3. Body - passes over the aorta and L2
  4. Tail - touches the spleen
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3
Q

What are the two FUNCTIONAL parts of the pancreas?

A
  1. Endocrine portion - produces hormones

2. Exocrine portion - produces digestive enzymes and alkaline fluid

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4
Q

What are the four cell types of the endocrine pancreas and what are their functions?

A
  1. Alpha - secrete glucagon for increasing BGLs
  2. Beta - secrete insulin for decreasing BGLs
  3. Delta - secrete somatostatin and gastrin
  4. F - secrete pancreatic polypeptide, for suppression of appetite in response to meal ingestion
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5
Q

What do the Islets of Langerhans do?

A

Lie between Acinar cells, produce and secrete hormones

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6
Q

Where do endocrine cells of the pancreas lie?

A

Adjacent to blood vessels to allow hormones to be secreted directly into circulation

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7
Q

Which cells make up the exocrine part of the pancreas? What do they secrete?

A

Acinar cells, secrete digestive enzymes:

  • Proteases, for breakdown of proteins
  • Amylase, for breakdown of carbohydrates
  • Lipase, for breakdown of fat into FFAs

Ductal cells, secrete:
- Alkaline fluid, for neutralising chyme and for fat digestion and absorption, released in response to secretin

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8
Q

How does the pancreas protect itself?

A
  • By secreting proteases in their inactive forms (zymogens)
  • Trypsin inhibitor - prevents early activation of proteases while in the pancreas
  • Alkaline fluids - flush enzymes into the duodenum
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9
Q

Pancreatitis is caused by?

A
I - Idiopathic
G - Gallstones
E - Ethanol/alcohol
T - Trauma
S - Steroids
M - Mumps/viruses
A - Autoimmune
S - Scorpion stings
H - Hypertriglyceridaemia/ hypercalcaemia
E - Endoscopic retrograde cholangiopancreatography
D - Drugs
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10
Q

Pathophys of pancretitis?

A

Unknown

Theory = injury to acinar cells = early activation of proenzymes causing autodigestion of the pancreas

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11
Q

What are the three phases of pancreatitis?

A
  1. Acinar cell injury
  2. Acute inflammatory response
  3. Systemic complications
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12
Q

What characterises phase 1 of pancreatitis?

A
  • Biliary tract obstruction = increases intraductal pressure, pancreatic juices back up and leak into interstitial tissue
  • Lipase causes fat breakdown = injury causes inflammatory response
  • Oedema = impairs blood flow = ischaemia
  • Proenzyme activation due to defective intracellular transport = pancreatic autodigestion
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13
Q

What characterises phase 2 of pancreatitis?

A
  • Injury to acinar cells and pancreatic tissue destruction = release of proinflammatory cytokines = inflammatory response
  • Inflammation leads to vascular changes and cellular events
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14
Q

What are the causes of primary acinar cell injury in pancreatitis?

A
  • Alcohol
  • Trauma
  • Viruses
  • Drugs
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15
Q

What vascular changes occur in phase 2 of pancreatitis?

A
  • Vasoconstriction due to histamine release
  • Vasodilation = increases hydrostatic pressure = pushes fluid into interstitial tissue
  • Increased vascular permeability = pushes exudate into interstitial tissue
  • Increased blood viscosity
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16
Q

What cellular events occur in phase 2 of pancreatitis?

A
  • Chemotaxis - movement of leukocytes towards the site of inflammation down a chemical gradient
  • Phagocytosis - leukocytes engulf and destroy dead cells
  • Activation of plasma protein systems
17
Q

Describe the steps that allow leukocytes to move from their place of origin to the site of pancreatitis?

A
  • Margination - movement of leukocytes from central axial column to the periphery
  • Rolling - Leukocytes move along the epithelial surface
  • Activation - Of adhesion molecules (selectins and integrins) on the surface of leukocytes
  • Adhesion - Leukocytes stick to the endothelial wall
  • Diapedesis - Movement of leukocytes from the endothelial wall to the interstitial tissue through gap junctions
18
Q

What are some systemic complications that occur in phase 3 of pancreatitis?

A
  • Shock
  • Cardiac - myocardial depression, decreased TPR, hypotension
  • Lungs - PO, ARDS
  • Renal - pre-renal failure, acute tubular necrosis
  • Sepsis
  • Disseminated intravascular coagulation - use of all clotting factors so pt continues to bleed
  • MODS
19
Q

Treatment for pancreatitis?

A

Fluid resuscitation

Vasopressors to vasoconstrict

20
Q

Clinical manifestations of pancreatitis?

A
  • Epigastric pain - central and upper abdo
  • N and V
  • Abdo distension and tenderness
  • Fever
  • Leukocytosis
  • Steatorrhea - excessive undigested fat in faeces due to lack of lipase
  • Transient hyperglycaemia - damaged alpha cells = release of glucagon = increased BGLs
  • Hypotension
  • Tachycardia
  • Hypoxaemia
  • Elevated urea and creatinine
21
Q

Diagnosis of pancreatitis?

A
  • Elevated serum amylase
  • Elevated serum lipase
  • Elevated urine amylase and serum CRP
  • Radioactive imaging
22
Q

Treatment of pancreatitis?

A

Does not exist

23
Q

Management of pancreatitis?

A
  • Fluid resuscitation + colloids - prevent hypovolaemia, increase TPR
  • Pain management - opioids, PCA
  • Nutrition - TPN for vomiting, NGT favourable, intake vs output charts
  • ABs - only if there is an infection
  • Surgery - pancreatic resection or removal of gallstones
24
Q

Chronic pancreatitis is due to?

A

Chronic alcohol abuse

25
Pathophysiology of chroinc pancreatitis?
Chronic inflammation leads to fibrosis, strictures, ductal obstruction and pancreatic cysts
26
How to manage chronic pancreatitis?
Lifestyle changes, pain relief, fat free diet