Where are pancreatic normally activated?

Where are they activated in pancreatitis?

duodenum

pancreas

(autodigestion, causes a huge amount of inflammation)

SPINK1 is on

This converts trypsinogen to trypsin.

The acute pancreatitis diagram also has high calcium. 

Symptoms of Pancreatitis

and

Signs

abdominal pain (midepigastric)

n/v

anorexia

abdominal distention

bowel sounds decreased

epigastric tenderness

low grade fever

tachycardia

grey-turner's sign

cullen's sign

amylase - elevated in 90% of cases

rises within 2-12 hours of sx, stays up 3-5 days

higher values suggest gallstone pancreatitis

Lipase

elevated for 5-7 days

usually values are in the 20-30 range; goes into the thousands for pancreatitis

elevated alanine aminotransferase (ALT)

suggestive of gallstone etiology

(generally, the CT will tell you this)

ultrasound - rules out cholelithiasis, pseudocyst

CT better imaging for pancreas

MRI

(these two are the tests of choice)

without necrosis

absence of organ dysfuntion

organ failure

local complications: necrosis, pseduocyst, abscess

risk factors for pancreatitis

On Admission

Age >55 years

WBC > 16,000 /mm3

Glucose > 200 mg/dl

Endocrine functions are failing

LDH > 350 units/L

AST > 250 units/L

48 hours after admission

Decrease Hct > 10%

Increase in BUN >5 mg/dl

Calcium < 8 mg/dl

PaO2 < 60 mm Hg

Base deficit > 4 mmol/l

Fluid deficit > 6 liters

Gallstones

alcohol (direct toxic effect and decrease in tubule perm)

drugs (2%)

didanosine

azathiprine/mercaptopurine

trauma

metabolic abnormalities

(hypertriglyceridemia, hypercalcemia)

infection

1. didanosine

possible accumulation of toxic metabolite

delayed onset - weeks to months after exposure

dose related

2. azathiprine/mercaptopurine

hypersensitivity reaction

typically one month post exposure

Can we replace it with a different agent?

Definite Association

1. Didanosine
2. Mercaptopurine

3. Azathioprine

4. Estrogens
5. Sulfonamides
6. Tetracycline
7. Valproic acid
8. Thiazides
9. Furosemide
10. Metronidazole
11. Methyldopa
12. Pentamidine
13. 5-Aminosalacylic acid
14. Sulindac

IV fluid and electrolyte replacement

maintain urine outut: 0.5-1.0 mL/kg/hr

therapies to rest the pancreas:

NPO, NG suction, IV H2 antagonist or PPI

(although NG tube may just cause more stress)

placement of feeding tube byond duodenum

appropriate in most cases

less incidence of complications that with parenteral nutrition

merperidine (but not really anymore)

morphine

hydropmorphone

fentanyl

PCA

Pseudocysts are a complication.

What are they?

a collection of pancreatic secreations

appears 2-3 weeks after initial attack

treatment:

50% resolve on their own

watch, reimage

persistent cyst needs drainage

generally due to hypoperfusion, autodigestion

pancreas is normally sterile tissue

risk of infection is high here

associated with higher mortality

develops in 40-70% of patients with pancreatic necrosis

leading cause of morbidity/mortality in pacreatitis

seen 1-4 weeks after initial onset

true/false

antibiotics are necessary in mild cases

enteric gram negative rods +/- anaerobes

enterococcus

carbapenems

others:

zosyn

3rd gen cephs (hold is good anaerobic coverage)

FQ + metronidazole

shock/cv collapse

coagulopathy

respiratory failur

acute renal failure