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Gastro > Pancreas 1: Acute and Chronic Pancreatitis > Flashcards

Pancreas 1: Acute and Chronic Pancreatitis Flashcards

1
Q

Protective mechanisms to prevent self digestion:

A
  • -production of enzyme in inactive form
  • -enclosed within membrane to protect against low levels of activated enzyme
  • -activated enzyme not co-localized with pro-enzyme
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2
Q

What stimulates release of zymogen from acinar cell?

A

VIP (neural, cAMP)
secretin (intestines, cAMP)
ACh (vagus, Ca++)
CCK (intestines, Ca++)

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3
Q

earliest event in the pathogenesis of acute pancreatitis

A

conversion of pancreatic zymogens to their active forms within the acinar cell

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4
Q

Mechanisms of pancreatic injury?

A
  1. blockage of secretions

2. co-localization of ZG + lysosomes, which leads to premature ZG activation and autodigestion

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5
Q

How do cytokines cause acute pancreatitis?

A
  1. Proteases activate complement
  2. C3a and C5a recruit PMNs and macrophages
  3. Inflammatory cells release cytokines (TNF-a, IL-1, PAF, and nitric oxide)

=Vascular injury and inflammatory responses

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6
Q

Local effects of acute pancreatic injurt

A
  1. Autodigestion of the pancreas
  2. Pancreatic swelling (edema)
  3. Fat necrosis and hemorrhage
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7
Q

Clinical manifestations of acute pancreatitis?

A

abd pain (radiating to back)

NV

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8
Q

Histopath of acute pancreatitis?

A

coagulative necrosis (with ghost cells) + hemorrhage + degenerating polys

fat necrosis between lobules

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9
Q

Gross pathology of acute pancreatitis?

A

fat necrosis between lobules

Severe acute hemorrhage

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10
Q

What is the function of circulating a1-antitrypsin?

A

inactivates circulating proteases

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11
Q

What is the function of circulating a-macroglobulin?

A

binds to circulating trypsin

facilitates monocyte clearance of macroglobulin-trypsin complexes

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12
Q

Severe Pancreatitis:

Fat saponification causes what clinical correlate?

A

hypocalcemia

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13
Q

Severe Pancreatitis:

phospholipase A2 causes what clinical correlate?

A

hypoxemia

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14
Q

Severe Pancreatitis:

kallikrein activation causes what clinical correlate?

A

hypotension

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15
Q

Severe Pancreatitis:

thrombin activation causes what clinical correlate?

A

DIC, hemorrhage

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16
Q

Severe Pancreatitis:

elastase + chymotrypsin cause what clinical correlate?

A

hemorrhage

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17
Q

Severe Pancreatitis:

TNF-alpha and IL-6 activation cause what clinical correlate?

A

fever
malaise
confusion

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18
Q

Acute Pancreatitis:

Main causes?

A

Gallstones and alcohol

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19
Q

Acute Pancreatitis:

Main symptoms?

A

abd pain, NV

20
Q

Acute Pancreatitis:

Diagnosis?

A

elevated serum amylase and lipase

inflamed pancreas on CT

21
Q

Acute Pancreatitis:

Trx?

A

VERY AGGRESIVE IV fluids

pain meds

remove stones if causitive

abx if biliary

NPO

22
Q

What causes hereditary pancreatitis?

A

Trypsinogen Mutation, which prevents its degradation

23
Q

Diagnostic criteria for acute pancreatitis?

A

Two of the following Three:

  1. abdominal pain, nausea/vomiting
  2. elevated serum amylase and lipase more than 3x upper limit of normal
  3. CT imaging showing pancreatic inflammation
24
Q

Factors Suggesting Gallstone Etiology?

A
  1. Age > 50
  2. amylase >4000 IU/L
  3. Female
  4. AST >100 U/L
  5. alk. phos. >300 IU/L
25
Q

Pancreatitis:

Predictors of Poor Outcome?

A

Admission hct >44% with failure to decr after 24h of IV fluids.

Admission BUN > 25 mg/dl with an incr after 24h of IV fluids.

(hct incr due to loss of plasma w/ retention of RBC)

26
Q

Which has a better prognosis: Interstitial Pancreatitis or Necrotizing Pancreatitis?

A

interstitial!

Necrotizing Pancreatitis has a multi-organ failure rate of 50%, infection rate 15-20%, mortality 17%

27
Q

Complications of Acute Pancreatitis

A

Fluid collections
Pseudocysts
Fistulas (ascites, pleural effusions)
Splenic vein thrombosis

28
Q

Chronic Pancreatitis:

Pathophysiology?

A

recurrent injury with tissue destruction and fibrosis

29
Q

Chronic Pancreatitis:

Cause?

A

chronic alcohol (80%)

30
Q

Chronic Pancreatitis:

Symptoms?

A

chronic abdominal pain, diabetes, steatorrhea

31
Q

Chronic Pancreatitis:Dx?

A

Imaging studies

32
Q

Chronic Pancreatitis:

Management?

A

Pain medications, insulin, enzyme supplements

33
Q

Chronic Pancreatitis: Pathophysiology, chr ETOH Ingestion

A

–> abn secretion –> protein plugs and ductal obst –> calcification, pain

–> recurrent bouts of pancreatitis –> stellate cell activation –> fibrosis –> pain + cell death (which causes malabs DM)

34
Q

Chronic Pancreatitis: Pathophysiology, Genetic Abn

A

–> recurrent bouts of pancreatitis –> stellate cell activation –> fibrosis –> pain + cell death (which causes malabs DM)

35
Q

Chronic Pancreatitis:

Histopath?

A 
lymphocytes
acini = gone
ducts still present (empty)
residual necrotic debris
early fibrosis
prolif/dysplasia of epith around duct
36
Q

Chronic pancreatitis: end-stage

Histopath?

A

replacement of exocrine acini and ducts by fibroadipose tissue, but with preservation of islets of Langerhans (because they don’t autodigest)

37
Q

Chronic Pancreatitis:

Clinical Presentation

A

Chronic abdominal pain
Malabsorption (steatorrhea)
Diabetes

**Malabsorption + DM = advanced stages

38
Q

Causes of Pain in Chronic Pancreatitis:

A
  • -Increased pressure from fibrosis
  • -Pseudocysts trying to expand against fibrotic area
  • -Neural Inflammation
39
Q

Pain Management in CP:

Any cause?

A

Narcotics

40
Q

Pain Management in CP:

Acute exacerbations?

A

abstinence

enzymes

41
Q

Pain Management in CP:

Neural inflammation?

A

nerve block splanchniectomy

42
Q

Pain Management in CP:

Ductal hypertension?

A

drainage (stent or surgery)

43
Q

Pain Management in CP:

Pseudocyst pressure?

A

drainage (stent or surgery)

44
Q

Steatorrhea in CP:

Cause?

A

lipase deficiency = fat malabsorption

45
Q

Steatorrhea in CP:

Trx?

A
  1. reduce dietary fat intake
  2. oral enzyme supplementation
  3. acid suppression therapy (for effectiveness of oral enzymes)
46
Q

Diabetes in CP:

Cause?

A

Only seen in severe disease with 80% destruction of pancreas:
Loss of both insulin and glucagon

47
Q

Diabetes in CP:

Is this easy to manage?

A

no–Loss of both insulin and glucagon = brittle

but low insulin requirements, and DKA is rare

Gastro (25 decks)

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