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Gen Med: GI > Pancreatic Disorders > Flashcards

Pancreatic Disorders Flashcards

1
Q

What is acute pancreatitis?

A
  1. Inflammation of pancreas that occurs suddenly & usually resolves in a few days w/ treatment
  2. Can be life-threatening w/severe complications
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2
Q

Causes of Acute Pancreatitis

A 
Gallstones
Chronic, heavy alcohol use
Abdominal trauma
Medications 
Infections
Tumors
Genetic abnormalities
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3
Q

Acute Pancreatitis: Etiology Theory

A

Develops when pancreatic enzyme outflow is obstructed, causing leakage of enzymes into pancreatic tissue
Leaked enzymes become activated leading to “autodigestion” of pancreatic tissue

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4
Q

Clinical Manifestations : Acute pancreatitis

A 
Fever
Leukocytosis
N/V may occur (↑ w/ paralytic ileus) 
Abd Pain
CBD obstruction (edema/stone)
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5
Q

Advanced Clinical Manifestations : Acute pancreatitis

A
  1. Abdominal distention
    a. Bowel hypomotility & accumulation of fluids in peritoneal cavity
  2. Hypotension & shock
    a. Plasma volume lost as enzymes released into circulation increase vascular permeability & dilate vessels
  3. Hypovolemia
  4. Azotemia
    Acute tubular necrosis (renal failure)
  5. Myocardial insufficiency
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6
Q

Severe Clinical Manifestations: Acute pancreatitis

A
  1. Small % of pts develop tachypnea & hypoxemia 2° to pulmonary edema, atelectasis, or pleural effusions caused by circulating pancreatic enzymes
  2. Multiple organ failure accounts for most deaths
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7
Q

Diagnostic Studies : Acute pancreatitis

A
  1. Serum Lipase ↑ 4-8 hr (nl 8-14 days)
  2. Serum Amylase ↑ 6-24 hr (nl 3-4 days)
  3. Trypsin-activated peptide (TAP); urine Trypsinogen & Carboxypeptidase B
    - All elevated (not widely available tests)
  4. ↑ CRP
  5. CBC
    a. Leukocytosis
    b. Hb/Hct may be ↑ 2° to 3rd space fluid loss
  6. CMP
    a. ↑ Serum Bilirubin 15-25% of cases 2° to pancreatic edema compressing CBD
    b. ↓ Serum Calcium
    c. +/- glucose
  7. (-) ETOH → USN & possibly Endoscopic Retrograde Cholangiopancreatography (ERCP)
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8
Q

What are the Severity of Dz classification systems?

A
  1. Ranson criteria
    - Used fornon-gallstone & gallstone pancreatitis, but parameters differ
    - Mortality increases w/ number of (+) signs
  2. Glasgow Prognosis Score
  3. APACHE III
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9
Q

Ranson Criteria : Non-gallstone pancreatitis parameters

A 
1. At admission:
Age > 55 years
White blood cellcount > 16,000 cells/mm3
Blood glucose> 200 mg/dL
SerumAST> 250 IU/L
SerumLDH> 350 IU/L
2. Within 48 hours:
Serum calcium < 8.0 mg/dL
Hctfall > 10% 
PaO2< 60 mmHg
BUN↑ by ≥ 5 mg/dL after IV fluid hydration
Base deficit > 4 mEq/L
Sequestration of fluids > 6 L
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10
Q

Ranson Criteria: Gallstone pancreatitis parameters

A 
1. At admission:
Age in years > 70 years
White blood cell count > 18,000 cells/mm3
Serum glucose> 220 mg/dL
SerumAST> 250 IU/L
SerumLDH > 400 IU/L
2. Within 48 hours:
Serum calcium < 8.0 mg/dL
Hct fall > 10%
PaO2< 60 mmHg
BUN↑ by ≥ 2 or more mg/dL after IV fluid hydration
Base deficit  > 5 mEq/L
Sequestration of fluids > 4 L
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11
Q

More Ranson Criteria

A 
1. Criteria at time of admission:
Age > 55 (1 point)
Glucose > 200 (1 point)
WBC > 16,000 (1 point)
AST > 250 (1 point)
LDH > 350 (1 point)
2. Criteria that may develop over 1st  48 hr:
BUN rises more than 5 mg/dL (1 point)
Base deficit > 4 (1 point)
Hct drops 10% or > (1 point)
PO2 < 60 (1 point)
Calcium < 8 (1 point)
Fluid sequestration > 6L (1 point)
 
Scoring
 ≥ 3 = acute severe pancreatitis              
 < 3 = acute mild pancreatitis
 0-2 points: Mortality = 1% 
 3-4 points: Mortality = 16% 
 5-6 points: Mortality =  40% 
 7-11 points: Mortality ≈100
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12
Q

Glasgow Prognosis Score (PANCREAS ACRONYM)

A 
PaO2 < 60mm Hg
Age > 55 yr 
Neutrophils: (WBC >15,000) 
Calcium < 8.0mg/dL 
Renal function:  	 		      (BUN > 49mg/dL)
Enzymes: (AST > 200 IU/L or  	   	           LDH > 600 IU/L)
Albumin < 32 gm/L
Sugar: (Glucose >200 mg/dL)
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13
Q

APACHE III Score

A
  1. ICU admission score only
    - Not pancreatitis specific
    - Not recalculated during hospitalization
  2. Calculated from patient’s age & 12 routinephysiologicalmeasurements
    - PaO2
    - Temperature (rectal)
    - Mean arterial pressure
    - pH arterial
    - Heart rate
    - Respiratory rate
    - Sodium
    - Potassium
    - Creatinine
    - Hematocrit
    - White blood cell count
    - Glasgow Coma Scale
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14
Q

Treatment: Acute pancreatitis

A
  1. Goal →stop autodigestion & prevent systemic complications
    a. NPO to “rest” pancreas
    b. Continuous gastric suction
    c. Narcotic medication for severe pain
    d. IV fluids essential to restore blood volume & prevent hypovolemia
    e. TPN to reverse the catabolic state
    f. PPI to↓ gastric acid production
  2. Monitor closely for complications
    a. Pancreatic pseudocyst
    → infection, hemorrhage, obstruction & rupture
    b. Renal failure
    c. Pleural effusion
    d. Hypocalcemia
    e. Pancreatic abscess
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15
Q

What is chronic pancreatitis?

A
  1. Inflammation of pancreas that does not heal or improve
    a. Worsens over time → permanent damage
  2. Irreversible damage to pancreas
    a. Assoc. w/ recurrent inflammation, fibrosis, & injury to the exocrine & endocrine tissues, causing episodes of pain
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16
Q

Causes: Chronic Pancreatitis

A
  1. Most common cause of chronic pancreatitis is many years of heavy alcohol use
  2. Can be triggered by 1 acute attack that damages the pancreatic duct → causes pancreas inflammation → scar tissue develops & slow pancreas destruction
  3. Other causes
    - Cholelithiasis
    - PUD
    - Hyperparathyroidism/Hypercalcemia
    - Hyperlipidemia/Hypertriglyceridemia
    - ERCP
    - Hereditary disorders (Cystic Fibrosis)
    - Smoking ↑ risk w/ ETOH abuse
17
Q

Signs & Sx’s : Chronic Pancreatitis

A
  1. Epigastric or diffuse abdominal pain
    a. +/- radiates through to back
    b. +/- postprandial
  2. Steatorrhea
  3. Loss of appetite
  4. Weight loss
  5. Nausea
  6. Vomiting
  7. Diabetes
  8. Malabsorption sx’s
    a. Diarrhea, bloating, pain
    b. Pancreatic calcification
    c. Steatorrhea
    d. DM
18
Q

Physical Exam: Chronic Pancreatitis

A

Evaluate for pallor, jaundice

Rarely, a tender fullness or mass may be palpated in epigastrium

19
Q

Diagnostic Studies : Chronic Pancreatitis

A
  1. Lab testing – most helpful during acute or advanced disease
    a. ↑ Alk phos/bilirubin if significant duct obstruction
    b. Serum amylase & lipase – normal to slightly ↑
    c. Serum Trypsin <10 ng/mL in advanced Dz
    d. Secretin-Caerulein test (SCT)
    - Gold Standard for pancreatic function
    e. Fecal testing
    - Quantitative fecal fat
    - Chymotrypsin
    - Pancreatic elastase 1
  • Pancreatic Calcification*
    2. Imaging
    a. Ultrasound (Endoscopic USN prn)
    b. CT scan
    c. ERCP (most sensitive)
    d. MRCP
20
Q

Secretin-Caerulein Test

A
  1. Combination of caerulein & secretin bolus given via gastrofiberscope
    a. Stimulate pancreatic exocrine secretion
    b. Measurement of duodenal juice
  2. Safe, reliable, & effective mean for the purpose of testing pancreatic function
21
Q

What is the classic triad of Chronic Pancreatitis?

A
  1. Pancreatic calc
  2. Steatorrhea
  3. DM
22
Q

Treatment: Chronic pancreatitis

A
  1. May require hospitalization:
  2. Pain management
  3. IV hydration
  4. Nutritional support – NG tube feedings may be necessary for several weeks for weight loss
  5. Synthetic pancreatic enzymes
    a. Taken w/ every meal to help food digestion & regain weight
23
Q

Management: Chronic Pancreatitis

A
  1. Low fat diet
  2. Avoid ETOH
  3. Smoking cessation
  4. Pain meds (avoid opiates if possible)
  5. Pancreatic supplements
    a. Containing Lipase, Amylase, Protease
    b. (Pancreaze, Creon, Ultresa, Zenpep)
  6. Surgery if indicated
    a. Resect pseudocyst, abscess, fistula, or fixed obstruction
  7. Corticosteroids for autoimmune Dz
  8. Insulin for DM
24
Q

Complications : Chronic Pancreatitis

A
  1. Opioid addiction
  2. Brittle DM
  3. Pseudocyst
  4. Abscess
  5. CBD stricture
  6. Steatorrhea
  7. Malnutrition
  8. PUD
  9. CA risk
    - 4% after 20 yr of Dz
    - 19% after age 50
25
Q

Pancreatic Insufficiency : Malabsorption

A

Inadequate metabolism of dietary substances due to defects in digestion, absorption, or transport

Interferes w/ nutrient absorption in small intestine

Results from mucosal disruption caused by

  • Gastric or intestinal resection
  • Vascular disorders
  • Intestinal Dz
  • Pancreatic insufficiency
26
Q

Pancreatic Insufficiency : Causes

A

Chronic pancreatitis
Pancreatic carcinoma
Pancreatic resection
Cystic Fibrosis

27
Q

Pancreatic Insufficiency: Diagnostic Studies

A 
Diagnosis made by pancreatic function testing (PFT)  
-Fecal fat 
-Fecal elastase
-Secretin-caerulein test (SCT)  
(Gold standard)

Management includes enzyme replacement & fat soluble vitamin therapy

28
Q

Pancreatic Cancer : Risk Factors

A 
ETOH abuse
Tobacco use
Increased age
Obesity
Long standing Hx of DM (1° in women)
Chronic pancreatitis
Heredity
29
Q

Pancreatic Cancer: Signs & Sx’s

A 
Painless jaundice**  
Epigastric pain
Weight loss
Anorexia
Pruritus
Nausea/Vomiting
Palpable liver
Clay colored stools
Courvoisier’s Sign*****
-Nontender, enlarged GB w/ jaundice
Trousseau Sign
Virchow’s Node
Blumer’s Shelf
Sister Mary Joseph Nodule
30
Q

Diagnostic Studies: Pancreatic Cancer

A 
CT , MRI, USN, ERCP, MRCP, PET scan
CBC
CMP (Alk Phos, GGT,AST, ALT)
Amylase, Lipase
CA 19-9 antigen to follow (not for screening)
CEA
31
Q

Treatment: Pancreatic Cancer

A
  1. Whipple Procedure (surgery)
    a. Factors that define inoperability
    - Vascular encasement
    - Liver Mets
    - Peritoneal implants
    - Distal lymph node mets

Surgery + chemotherapy & external beam radiation

  • 40% 2-yr survival
  • 25% 5-yr survival
32
Q

Insulinoma

A

Rare pancreatic beta cell tumor that hypersecretes insulin (Hyperinsulinism)

Whipples Triad
Low serum glucose (<50 mg/dL)
CNS symptoms of hypoglycemia
Eating carbohydrates relieves symptoms

Treatment
Surgical resection

33
Q

Gastrinomas (AKA Zollinger-Ellison Syndrome)

A

Z-E syndrome caused by a gastrin-producing tumor usually located in the pancreas, duodenal wall, or lymph nodes

Gastric acid hypersecretion by parietal cells & gastric/peptic ulcerations result

Sx’s-pain, chronic diarrhea, steatorrhea, weight loss, hematemesis

Diagnosis -fasting serum gastrin levels x 3(normal < 100 pg/ml) or Secretin stim test, MRI to R/O tumor

Treatment
-PPI & surgical resection

34
Q

Vipoma

A
  1. Malignant pancreatic islet cell tumor secreting vasoactive intestinal peptide (VIP)→
    a. Syndrome of extreme Watery Diarrhea, Hypokalemia, and Achlorhydria* (WDHA syndrome)
    - *Production of gastric acid in the stomach is absent or low

Diagnosis-serum VIP levels

Tumor is localized w/ CT & endoscopic USN

Treatment
-Surgical resection

35
Q

Glucagonoma

A

Rare malignant islet cell tumor originating from alpha-2 cells that secrete glucagon

Causes hyperglycemia & characteristic skin rash

  • Found on shin, face, & groin
  • Necrolytic migratory erythema

Diagnosis is by ↑ glucagon levels & imaging studies
-Tumor localized w/ CT & endoscopic USN

Treatment
Surgical resection

Gen Med: GI (9 decks)

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