kale pancreatitis

endocrine pancreatic fxns

1. release insulin (glucose uptake and glycogen deposition)

2. release glucagon (converts glycogen to glucose)

somatostatin== inhibits glucagon and insulin, reduces pancreatic secretions

which pancreatic cells secrete water, electrolytes, and digestive enzymes

acinar cells

how is pancreatic secretion regulated

1. cephalic phase= sight/smell via vagus nerve (VIP and GRP)

2. intestinal phase

3. hormones== secretin, cholecystokinin

presence of acid in duodenum triggers release of ________

_______ causes release of bicarb

presence of fats in duodenum triggers release of _________

________ triggers release of enzymes

presence of acid in duodenum triggers release of __secretin__

_secretin__ causes release of bicarb

presence of fats in duodenum triggers release of __cholecystokinin___

__cholecystokinin___ triggers release of enzymes

why arent proenzymes automatically activated in pancreas? how do they get activated?

-pancreatic juices have a low level of trypsin inhibitor that stops early activation

- need ENTEROKINASE to activate TRYPSINOGEN which activates enzymes

_______________ activates ___________ which activates pancreatic enzymes

enterokinase; trypsinogen

which drugs are associated with acute pancreatitis

corticosteroids, ACE inhibitors, estrogen, furosemide, codeine, sulfasalazine, Bactrim, sulindac, carbamazepine, isoniazid

incretin based= liraglutide, exenatide, sitagliptan

+ others

gold standard dx of pancreatitis

surgical examination of pancreas

lab parameters of pancreatitis

-leukocytosis (necrosis-> infection-> WBCs)

- hyperglycemia (less insulin)

- increased BUN/Cr

- PT prolongation

- hyperbilirubinemia

- hypocalcemia

- thrombocytopenia

- increased Hbg/Hct

- hypoalbunemia

describe what happens to serum amylase during acute pancreatitis

increases within 24hrs of sx onset, return to normal over 3-4 days

t/f: amylase levels dont correlate to pancreatitis severity and are not specific to the pancreas

true

[compare to lipase which is specific and 7-10 days]

which serum enzyme is specific to pancreatitis and persists longer

serum lipase= specific to pancreas and persists 7-10 days

what dx technique is indicated for pts with suspected biliary involvement

ultrasound

what dx technique is useful in classifying pancreatitis severity and provides an estimate of risk for systemic complications

contract enhanced computer tomography (CECT)

t/f: there is greater mortality with first attacks of pancreatitis than with recurrent

true

severity and mortality of pancreatitis pts is predicted by

Ranson's criteria

ex: age over 55, WBC, glucose, LDH, etc

phlegmon

mass of inflamed pancreas with patchy areas of necrosis

pseudocyst

cysts with no epithelial lining and most common chronic complication

-> fluid collections of necrotic debris, blood, and pancreatic enzymes

[must be drained]

manifestations of acute pancreatitis include

-hypotension/shock (main cause of death)

-HYPOcalcemia (think of using up Ca to activate enzymes)

-HYPERglycemia

- renal failure

- pulmonary edemas

- coagulopathy

what kind of route is indicated for pancreatitis tx

1. stop ingesting food/liquid [to stop stimulating pancreas]

2. En preferred==NG tube

- TPN INDICATED IF ON BOWEL REST FOR 1 WEEK

3. replace fluid/electrolyte losses

what kind of analgesics are indicated for acute pancreatitis

IV PREFERRED FOR ACUTE ATTACK

1. meperidine 50-100mg IV q4hrs and prn

-CI in renal failure, not rlly used bc seizures

2. morphine

3. hydromorphone (especially in renal insufficiency)

abx and acute pancreatitis tx

- NO benefit as prophylaxis in ethanol induces pancreatitis

- can use abx for pancreatic duct obstruction or abscess/necrotizing

which abx are recommended for secondary infections

1. imipenem 500mg IV q8hrs (covers gram neg and penetrates pancreas)

- NOT FOR PCN ALLERGY (beta lactam)

2. Cipro 400mgIV q12hrs + metro 500mg IV q 8hrs

t/f: H2RAs are the most effective in decreasing GI secretions in pancreatitis

false. not more effective than NG suction

acute pancreatitis tx summary

analgesics

- morphine or hydromorphone

- less preferred: meperidine 50-100mg IV q4hrs/prn

abx

- not needed as prophylaxis in alcohol induced

- can be used in pancreatic duct obstruction/ abscess/ necrotizing

1. imipenem 500mg IV q8hrs (covers gram neg and penetrates pancreas)

- NOT FOR PCN ALLERGY (beta lactam)

2. Cipro 400mg IV q12hrs + metro 500mg IV q 8hrs

t/f: chronic pancreatitis results in functional and structural damage to the pancreas and is irreversible

true

etiologies of chronic pancreatitis

alcohol

hyperparathyroidism (Ca activating all the proenzymes)

PCM (not enough protein)

heredity

trauma

duct obstruction

chronic pancreatitis clinical presentation

1. dull constant pain, epigastric and radiating through back

may be accompanied by N/V and weight loss

2. malabsorption= >7g of fat in feces-> steatorrhea and azotorrhea

- B12 malabsorption

-> diabetes, weight loss, jaundice

clinical triad of chronic pancreatitis dx

Chronic Disease Suck

calcification, steatorrhea, diabetes (10-20yrs of alcohol use)

t/f: serum amylase and lipase not useful in diagnosing chronic pancreatitis

true. lipase useful in acute only. amylase not rlly useful

gold standard diagnosing technique for chronic pancreatitis

ERCP (endoscopic retrograde cholangiopancreatography)

diet tx for chronic pancreatitis

- abstain from EtOH

- eat small and frequent meals (6/day)

- restrict fat (80-100g/day)

analgesics for chronic pancreatitis

- aspirin or tylenol before meals

- use around the clock!!

- opiates for severe pain (oral before parenteral)

celiac plexus block

Pain management technique for chronic pancreatitis

- injection of alcohol into celiac ganglion (3-6 month relief)

summary of chronic pancreatitis tx

1. diet= stop alcohol, eat small frequent meals with low fat

2. use aspirin or tylenol around the clock

- try opioids if rlly needed

3. enzyme replacement

4. celiac plexus block

how should lipase enzyme supplement be given/ what should be considered

lipase is irreversible inactivated at pH<4, can give H2RA/PPI to not degrade the exogenous enzyme

max delivery of lipase after a meal

140k IU for 4hrs

malabsorption is minimized if the concentration of lipase delivered to duodenum is at least __% of normal max

this means you need _______IU of lipase and ______IU of trypsin during 4hrs after meal

5%

30k IU lipase every meal and 10k IU trypsin

which brand of enzymes are not EC and must be taken with a PPI

Viokase

(others that are EC: pancreaze, creon, zenpep, pertzye, ultresa)

ADEs of supplemental enzymes? monitoring?

hyperuricosuria

hyperuricemia

kideny stones

folic acid deficiency

===monitor uric acid and folic acid levels!

to treat steatorrhea:

begin with pancreatic enzyme supplement: ______units/meal

if dose increase needed: ____ units/meal

if no improvement?

25k-50k/ meal

increase to max of 90k units/meal

add H2RA or PPI and reduce dietary fat

max dose of enzymes

90k units per meal

opioids for chronic pancreatitis

tramadol 50-100mg q4-6hrs

codeine, hydrocodone, morphine sulfate, oxycodone, methadone, hydromorphone

monitoring parameters for pancreaze and counseling

30,000 IU q4 hrs

may cause kidney stones

monitor: folic acid and uric acid levels