16. pancreatic disease

acute inflammation of the pancreas due to premature activation of pancreatic enzymes

define acute pancreatitis

Per the Revised Atlanta Classification:

Moderately severe acute pancreatitis = transient organ failure (<48 hours) and/or local or systemic complications, WITHOUT persistent organ failure.

Examples of local complications:

• Pancreatic/peripancreatic fluid collections

• Pancreatic necrosis

• Pseudocyst

• Walled-off necrosis

Severity classification

Severity	Definition
Mild	No organ failure and no local/systemic complications
Moderately severe ⭐	Transient organ failure <48 hr and/or local/systemic complications
Severe	Persistent organ failure >48 hr

48 time marker:
<48 hr = moderate
>48 hr = severe

define moderately severe acute pancreatitis

Persistent organ failure (>48 hrs)

define severe acute pancreatitis

gallstones

• _{Gallstone travels from gallbladder → common bile duct → gets impacted near the ampulla of Vater → obstructs pancreatic drainage → premature pancreatic enzyme activation → autodigestion/inflammation of the pancreas.}

both uses the common bile duct

most common overall cause of acute pancreatitis

ethanol

most common cause of pancreatitis in the US

GET SMASHED

Gallstones

Ethanol

Trauma

Steroids

Mumps (viral)

Autoimmune

Scorpion sting (&brown rec. spider/lizard)

Hypertriglyceridemia (>1000)

ERCP

Drugs (azathioprine, valproate, thiazides)

mnemonic for risk factors for pancreatitis

GET SMASHED

>1000s

TG level causing pancreatitis

azathioprine, valproate, thiazides

drugs associated with pancreatitis

transient obstruction of ampulla of vater

how do gallstones cause pancreatitis

direct acinar injury + ↑ viscosity of secretions

how does alcohol cause pancreatitis

trypsin

premature activation of ________ --> autodigestion of the pancreas

Acinar cell injury or duct obstruction

Trypsinogen → trypsin (inside pancreas)

Activation of other enzymes (lipase, elastase)

Autodigestion + inflammation

Fat necrosis → ↓ calcium (saponification)

Systemic inflammation → SIRS → organ failure

pathophysiology of acute pancreatitis

Severe epigastric pain that radiates to the back

worse after eating

Nausea/vomiting

classic presentation of acute pancreatitis

Epigastric tenderness

Abdominal distension (ileus)

physical exam findings associated with pancreatitis

bruising around umbilicus (pancreatitis or ectopic pregnancy)

nonspecific: intra-abdominal bleeding

Grey Turner sign

ecchymoses of the flanks associated with fulminant hemorrhagic pancreatitis; very poor prognostic sign

nonspecific: retroperitoneal bleeding

requires 2/3:

• epigastric pain

• Lipase or amylase ≥3× normal (lipase preferred)

• Imaging (CT/MRI) showing pancreatitis

*if first two are positive, you do NOT need a CT to confirm dx

diagnostic criteria for acute pancreatitis

gallstone pancreatitis

• ALT >150 U/L strongly suggests a biliary/gallstone etiology

• May have ↑ bilirubin/ALP if persistent biliary obstruction

elevated AST/ALT in the setting of pancreatitis, think

Calcium finding	Relationship to pancreatitis
Hypercalcemia ↑ Ca²⁺	Can CAUSE acute pancreatitis ⭐ — classically from hyperparathyroidism
Hypocalcemia ↓ Ca²⁺	Can RESULT FROM severe acute pancreatitis ⭐

_{Why does calcium DROP in pancreatitis?}

• _{Pancreatic enzymes cause fat necrosis → free fatty acids bind calcium → form insoluble calcium soaps. (saponification)}

• _{Pancreatitis → fat necrosis → saponification → ↓ serum Ca²⁺}

** can also see low Mg with necrosis (fats), but low Ca is a worst prog

calcium labs associated with pancreatitis

(hyper vs hypo)

1. NPO

2. aggressive IV fluids (lactated ringers). _{- inflame —> leaks fluids —> fluids saves renal/BP status}

3. pain control (hydromorphone)

MILD IMPROVES WITHIN 2-3DAYS

core management of acute pancreatitis

YES —

Early enteral feeding (within 24–48 hrs if tolerated)

Avoid prolonged NPO

are you NPO with acute pancreatitis?

NOT routine

Only if:

• infected necrosis

• cholangitis

are abx indicated for acute pancreatitis?

Situation	ERCP?
Acute cholangitis ⭐	YES — urgent ERCP
Persistent common bile duct (CBD) obstruction	YES
CBD stone seen on imaging	YES
Persistent jaundice / rising bilirubin suggesting obstruction	YES
Gallstone pancreatitis without cholangitis or persistent obstruction	❌ No routine ERCP
Alcohol-induced pancreatitis	❌ No

Gallstone pancreatitis alone ≠ indication for ERCP.

_{—> for JUST gallstone pancreatitis —> just take out the dang GB}

indications for ERCP in acute gallstone pancreatitis

fat necrosis

decreased calcium in pancreatitis signifies

with antibiotics that penetrate necrotic tissue and use a step-up approach:

• drainage first,

• then debridement only if needed.

  • Debridement is usually delayed about 4 weeks when possible because early debridement increases morbidity and mortality

treatment of pancreatic necrosis

peripancreatic fluid collections

-complicaiton of pancreatitis: early

• Fluid accumulation around the pancreas (no defined wall)

• most resolve without intervention, drain if infected

pancreatic pseudocysts

-complicaiton of pancreatitis

• a delayed, encapsulated fluid collection without solid necrotic debris

• usually after ~4 weeks after pancreatis episode

• drain if infected/sympotmatic, otherwise it will reslove

results from duct disruption or pseudocyst leak

causes of pancreatic ascites

(-complicaiton of pancreatitis)

ERCP with transpapillary pancreatic duct stenting

treatment of persistent pancreatic ascites

Many external pancreatic fistulas close with conservative care;

—> persistent or refractory fistulas may benefit from ERCP with sphincterotomy and pancreatic duct stenting

management of pancreatocutaneous fistula

(-complicaiton of pancreatitis)

pseudoaneurysm

most likely vascular complication of pancreatitis

*calcium under 8 is very bad

base def is 24- bicarb (>4 is very low bicarb)

Ranson's admission criteria

(for non-gallstone pancreatitis)

predicts mortality outcomes

Pathology	Repeated inflammation → irreversible fibrosis + destruction of pancreas → loss of exocrine and eventually endocrine function
Etiology	Chronic alcohol use (common); smoking, recurrent acute pancreatitis, genetic causes (CF, PRSS1), pancreatic duct obstruction, autoimmune pancreatitis
Presentation	Chronic/recurrent epigastric pain radiating to back, weight loss, steatorrhea, malabsorption (ADEK) → later diabetes
Diagnosis	CT abdomen → pancreatic calcifications, atrophy, dilated/irregular pancreatic duct; MRCP/EUS if CT unclear
Labs	Amylase/lipase may be normal because pancreas is fibrotic; fecal elastase ↓ with exocrine insuff.
General treatment	Stop alcohol + smoking, nutrition, pancreatic enzyme replacement, fat-soluble vitamins as needed; treat diabetes
Chronic pain management	Stepwise: alcohol/smoking cessation → non-opioid analgesics → pancreatic enzymes in selected patients → endoscopic therapy for duct stones/strictures → surgery for refractory obstructive pain
Endoscopic treatment	ERCP-based stone removal/stenting for selected pancreatic duct obstruction/strictures
Surgery	Persistent severe pain/duct obstruction despite medical/endoscopic therapy → drainage or pancreatic resection depending on anatomy

Board buzzwords: Chronic pancreatitis = pancreatic calcifications + chronic epigastric pain + steatorrhea + diabetes.

define chronic pancreatitis

#1 alcohol,

& smoking, genetic causes, obstructive disease, autoimmune pancreatitis, recurrent acute pancreatitis, and idiopathic disease

major causes of chronic pancreatitis

exocrine

are most pancreatic cancers exocrine or endocrine?

---

recall:

	Exocrine pancreas	Endocrine pancreas
Main job	Digestion	Blood glucose regulation
Structure	Acinar + ductal cells	Islets of Langerhans
Where secreted?	Into pancreatic ducts → duodenum	Directly into bloodstream
Acinar cells	Digestive enzymes	—
Ductal cells	HCO₃⁻ (bicarbonate)	—
α cells	—	Glucagon ↑ glucose
β cells	—	Insulin ↓ glucose
δ cells	—	Somatostatin
PP/F cells	—	Pancreatic polypeptide

pancreatic ductal adenocarcinoma

---

Classic board presentation

Older patient + weight loss + painless jaundice + palpable nontender gallbladder
→ Pancreatic adenocarcinoma in the head of the pancreas

Genetics to memorize

KRAS → CDKN2A → TP53 → SMAD4

CA 19-9: useful for following known disease/treatment response, but not a screening or stand-alone diagnostic test.

Feature	High-yield finding
Most common location	Head of pancreas ⭐
Major risk factor	Cigarette smoking; age >50yrs, DM, chronic pancreatitis, obesity, diabetes, family/genetic syndromes
Common mutations	KRAS ⭐, TP53, CDKN2A (p16), SMAD4
Tumor marker	CA 19-9 ⭐ — mainly monitoring, not screening
Head tumor presentation	Painless obstructive jaundice ⭐, dark urine, pale stools, pruritus
Body/tail presentation	Often presents later → abdominal/back pain, weight loss
Gallbladder	Courvoisier sign = palpable, nontender gallbladder + jaundice
Other clue	Trousseau syndrome = migratory thrombophlebitis
Diagnosis/staging	(u/s first) Pancreas-protocol contrast CT
Definitive treatment	Surgical resection if resectable + systemic chemotherapy pallitive: bile stent to remove jaundice
Head tumor surgery	Whipple procedure (pancreaticoduodenectomy)
Body/tail surgery	Distal pancreatectomy, often with splenectomy

associated with BRCA2 (jews)

ASSOCIATED WITH CHRONIC PRANCEATITIS BUT NOOOOTTT ALC DRINKING!!

most common malignant pancreatic cancer

PAINLESS JAUNDICE

• dark urine/light stools,

• epigastric or back pain,

• weight loss, anorexia, and fatigue

• courver’s sign (nontender, enlarged GB)

• Trousseu’s syndrome

symptoms associated with pancreatic cancer

Whipple (pancreaticoduodenectomy)

surgery for pancreatic cancer of the head lesions

a major surgery to remove the:

• head of the pancreas,

• the first part of the small intestine (duodenum),

• the gallbladder, and part of the bile duct

what does the whipple procedure remove?

distal pancreatectomy

surgery for body/tail pancreatic cancer

Tumor	High-yield features
Pancreatic ductal adenocarcinoma (PDAC) ⭐⭐⭐	Most common pancreatic malignancy; usually head; painless jaundice, weight loss; CA 19-9; KRAS, TP53, SMAD4, CDKN2A
Pancreatic neuroendocrine tumors (PanNETs)	Arise from islet/endocrine cells; can be functional or nonfunctional
→ Insulinoma ⭐	Most common functional PanNET; hypoglycemia → Whipple triad
→ Gastrinoma	↑ gastrin → Zollinger-Ellison → refractory/multiple ulcers + diarrhea; associated with MEN1
→ Glucagonoma	Diabetes + necrolytic migratory erythema ⭐
→ VIPoma	WDHA = watery diarrhea, hypokalemia, achlorhydria
→ Somatostatinoma	Diabetes + gallstones + steatorrhea
Solid pseudopapillary neoplasm	Classically young women; large well-circumscribed tumor; generally favorable prognosis
Serous cystadenoma	Usually benign; microcystic/honeycomb appearance + central scar
Mucinous cystic neoplasm (MCN) ⭐	Usually women, body/tail; ovarian-type stroma; malignant potential; does NOT communicate with pancreatic duct
IPMN ⭐	Mucin-producing tumor that communicates with pancreatic duct; malignant potential

1. PDAC → most common overall; head + painless jaundice + CA 19-9

2. Insulinoma → hypoglycemia + Whipple triad

3. Gastrinoma → MEN1 + Zollinger-Ellison

4. MCN → woman + body/tail + no duct communication

5. IPMN → mucin + pancreatic duct communication

6. Serous cystadenoma → benign + central scar/honeycomb

Quick distinction:
PDAC = exocrine cancer
PanNETs = endocrine tumors
MCN/IPMN/serous cystadenoma = cystic pancreatic neoplasms.

pancreatic tumors to be aware of

• Early: less than 4 weeks after acute episode

  • Acute peripancreatic fluid collection

  • Acute necrotic collection

• Late: more than 4 weeks after acute episode

  • Pancreatic pseudocyst

  • Walled-off necrosis

Pancreatic Complications

• All identified based on contrast-enhanced CT criteria

• Early: less than 4 weeks after acute episode

  • ____________________

  • ____________________

• Late: more than 4 weeks after acute episode

  • __________________

  • ___________________

• Treatment based on severity/symptoms:

  • Observation

  • Drainage

  • Surgery

… just so you can see it together what complications you might want on your ddx