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
Q

Pathophysiology of chroinc pancreatitis?

A

Chronic inflammation leads to fibrosis, strictures, ductal obstruction and pancreatic cysts

26
Q

How to manage chronic pancreatitis?

A

Lifestyle changes, pain relief, fat free diet