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GI Week 3 > Lecture 31: Acute and Chronic Pancreatitis > Flashcards

Lecture 31: Acute and Chronic Pancreatitis Flashcards

1
Q

What is acute pancreatitis?

A

A CHEMICAL BURN
An intraabdominal burn
Acute inflammation of the pancreas and associated adjacent organs without evidence of chronic pancreatitis

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2
Q

What is the Atlanta symposium of acute pancreatitis?

A

2 of 3 need to be present

  1. Typical pancreatic type pain
  2. Radiographic findings of acute pancreatitis
  3. Elevations in blood chemistries (typically amylase or lipase)
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3
Q

What are the histological features of pancreas?

A

No acini
Infiltration of polys all over
Necrosis

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4
Q

What are the basic clinical features of acute pancreatitis?

A
  1. severe pain (upper abdomen and radiate into back)
  2. starts quickly (10-20 mins) and lasts days
  3. 90% vomit
  4. 5-10% is painless!
  5. fevers occur even in the absence in infection!
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5
Q

What are the complications of acute pancreatitis?

A
  1. Early

2. Late (usually infection)

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6
Q

What are the types of early acute pancreatitis?

A
  1. cholangitis (fever, RUQ, jaundice)
  2. hypotension (cuz all the fluid is flowing to the pancreas)
  3. Systemic inflammatory response (SIRS)
  4. Renal failure
  5. Third spacing/ascites (refers to situation in which fluid shifts out of blood into a body cavity or tissue where it is no longer available as a circulating fluid, ie peritonitis)
  6. hypoxia (because fluid in the lungs)
  7. Hypocalcemia (because lipase breakdown fat, negative charge attracts calcium, brings about saponification, so you get “soap” in pancreas)
  8. Death from the fact that you have HYPOcalcemia from pancreatitis
    ORGAN SHUTDOWN
    Remember saponification
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7
Q

What are the late types of acute pancreatitis?

A
  1. splenic vein thrombosis (gastric varices)

2. infected necrosis and abscess

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8
Q

How do the acute pancreatitis complications come about?

A

Trypsin is activated
Autodigests and leaks out even more trypsin zymogen
Polys come rushing in
Neutrophil elastase is released, thereby recruiting a shitload of neutrophils
Fluid comes rushing in because the endothelium becomes leaky
Fluid then leaks into the lungs

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9
Q

What are the etiologies of acute pancreatitis?

A
  1. Alcoholic
  2. Biliary
  3. idiopathic
  4. Other (like ischemia, trauma, ERCP, neoplasia lol, metabolic causes like hypertriglyceridenemia, autoimmune)
  5. IgG4 = autoimmune, common in Asians
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10
Q

What are the characteristics of biliary etiology?

A
  1. comes from gallstones or sludge
  2. most common etiology of pancreatitis in worl
  3. obstruction at major papilla
  4. because of obstruction, bile goes up the pancreatic ducts and bile triggers inflammatory response (because they usually don’t see bile)
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11
Q

What is the pathophysiology of EtOH damage?

A
  1. changes pancreatic blood flow (poor blood flow)
  2. Radical production by necrosis of lysosomes = ROS injury of pancreas
  3. Sensitization of acini to CCK, leads to zymogen activation/cytokine generation
  4. causes spasm of sphincter of Oddi to lead to acute obstructive injury
    Hypothetical shit
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12
Q

Where is CCK made?

A

“I”-cells of the duodenum

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13
Q

What are important things to know about hypertriglyceridemia as a cause of acute pancreatitis?

A

Patients have HYPERglycemia

Can have NORMAL amylase and lipase

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14
Q

What is the recommendation for a patient who has unexplained pancreatitis over the age of 50?

A

Should have CT 6 weeks later

This is because it could be a cancer!!

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15
Q

What is the pathophysiology of acute pancreatitis?

A

Premature/intracellular activation of trypsin
Trypsin is the major catalyst for pancreatitis
Leads to activation of chymotripsinogen, trypsinogen, elastase, phospholipase A2
Then leads to autodigestion

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16
Q

What are the characteristics of trypsin?

A

Trypsin = PRSS1
Has an autolysis loop (R122)
Mutation in autolysis loop (R122) means you cant inactivate trypsin
Activated by CALCIUM
Has SPINK1 portion that inactivates trypsin (PSTI)
Any mutation to SPINK1 = activation of trypsin

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17
Q

What activates the zymogens from pancreas?

A

Enterokinase from the enterocytes converts those

Inactive enzymes to active ones (trypsin)

18
Q

What upregulates digestion?

A
  1. bile
  2. low pH
  3. trypsin
  4. high calcium, triglyceride
  5. CCK
  6. vagal stimulation
19
Q

What downregulates trypsin/digestion?

A
  1. SPINK1

2. somatostatin

20
Q

What triggers zymogen activation/generation of inflammatory mediatrs/ischemia?

A

Insult/trauma

Exacerbated by obesity and smoking

21
Q

How do you manage acute pancreatitis?

A

NPO/IV fluids/pain control

Bunch of tests to rule out need for surgery, etc

22
Q

What is chronic pancreatitis?

A

Permanent damage to the pancreas

Exocrine/endocrine dysfunction or destruction of such tissue on biopsy

23
Q

How do you know there is chronic pancreatitis?

A
  1. calcifications
  2. pancreatic duct stones
  3. dilated irregular pancreatic duct without mass
  4. beads on a string
  5. atrophy without mass
24
Q

What do calcifications and stones in pancreatic duct suggest?

A

Chronic pancreatitis

25
Q

What is the spectrum of chronic pancreatitis symptoms?

A
  1. minimal change/small duct
  2. structural damage
  3. steatorrhea
  4. diabetes
26
Q

What is the etiology of CP?

A
  1. Alcohol

2. tobacco

27
Q

What are the histological features of CP?

A

Fibrosis

Monos

28
Q

What is the test for chronic pancreatitis?

A

Secretin stimulation test
Measures pancreas secretion by injecting extraneous secretin
If juice is below 80 in terms of content, then you have chronic pancreatitis

29
Q

What are the hypotheses of chronic pancreatitis pathophys?

A
  1. Ductal obstruction hypothesis
  2. Toxic/metabolic hypothesis
  3. Necrosis/fibrosis
30
Q

What is the ductal obstruction hypothesis?

A

Protein precipitates/calcifications in ducts activates trypsin
Apoptosis/fibrosis of upstream acini

31
Q

What is the toxic/metabolic hypothesis?

A

Oxidative stress, free radicals from EtOH, CCK stimulation

Stellate cell activation/fibrosis

32
Q

What is the necrosis/fibrosis hypothesis?

A

Acute inflammatory attacks lead to necrosis/apoptosis and via cytokines from macrophages
Lead to chronic damage by converting to anti-inflammatory fibrotic/healing state
Fibrosis leads to local ischemia, causing more necrosis/apoptosis
Similar to a keloid

33
Q

What is ERCP?

A

Endoscopic RetroCholangioPancreatography

Can cause acute pancreatitis

34
Q

What is MRCP?

A

Magnetic Resonance CholangioPancreatography

35
Q

What are the consequences of chronic panc?

A
  1. pain
  2. steatorrhea
  3. diabetes
  4. osteoporosis
  5. biliary obstruction, B12 deficiency, cancer
36
Q

What are the causes of pain in chronic pancreatitis?

A

Amylase and lipase can be low so hard to detect

  1. neural pain
  2. obstructed pancreatic duct with panc stones
  3. malabsorption (cramps)
37
Q

What is the treatment for chronic pancreatitis?

A
  1. high dose nonenteric coated pancreatic enzymes
  2. quite EtOH and tobacco
  3. neural modulators
  4. narcotics
  5. ERCP to remove pancreatic stones/dilate strictures
  6. Surgery
38
Q

What is type 3 diabetes?

A

Diabetes caused by chronic hepatitis
EVERYTHING in the islets are fucked up
No glucagon + no somatostatin in addition to no insulin
Therefore, patient presents with hypoglycemic diabetes
No ketoacidosis
Still use metformin

39
Q

What is the difference between pancreatic diabetes and regular diabetes?

A

Pancreatic diabetes = HYPOglycemia in blood
-thin, adult onset
Regular diabetes = HYPERglycemia in the blood
-not likely to be thin (mostly obese)

40
Q

What are the two mortality peaks of acute pancreatitis?

A
  1. EARLY from organ failure

2. LATE from infection

41
Q

When does steatorrhea occur?

A

When you reach 10% of normal lipase level
So you can lose 90% of lipase levels and still function….once you get only 9% of lipase concentration, then you get steatorrhea

GI Week 3 (11 decks)

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