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Gen Med: GI > Pancreatic Disorders > Flashcards

Pancreatic Disorders Flashcards

1
Q

Define 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

What is the etiology of pancreatitis?

A
  1. Gallstones
  2. Chronic, heavy alcohol use
  3. Abdominal trauma
  4. Medications: GLP1 agonists
  5. Infections
  6. Tumors
  7. Genetic abnormalities
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3
Q

What is Acute (hemorrhagic) pancreatitis?

A
  1. Usually mild Dz

2. About 20% develop severe pancreatic inflammation requiring hospitalization

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4
Q

What is the thoery of pathophys of acute pancreatitis?

A
  1. Develops when pancreatic enzyme outflow is obstructed, causing leakage of enzymes into pancreatic tissue
  2. Leaked enzymes become activated leading to “autodigestion” of pancreatic tissue
  3. Gallstone obstruction is a contributing factor
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5
Q

What are the sxs of acute pancreatitis?

A 
A. Early sxs
1. Fever
2. Leukocytosis
3. N/V may occur (↑ w/ paralytic ileus) 
4/ Abd Pain
5. CBD obstruction (edema/stone)
B.Advanced signs
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
5. Acute tubular necrosis (renal failure)
6. Myocardial insufficiency 
C. Severe clinical sxs
1. Small % of pts develop tachypnea & hypoxemia 2° to pulmonary edema, atelectasis, or pleural effusions caused by circulating pancreatic enzymes
  1. Multiple organ failure accounts for most deaths
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6
Q

What are the laboratory dx studies for 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
    A. 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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7
Q

What are the Clinical predictors measuring severity ofacute pancreatitis
and Severity-of-Dz classification systems for acute pancreatitis?

A
  1. Ranson criteria
  2. Glasgow Prognosis Score
  3. APACHE III
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8
Q

When is ranson criteria used?

A
  1. Used for non-gallstone & gallstone pancreatitis, but parameters differ
  2. Mortality increases w/ number of (+) signs
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9
Q

What are the non-gallstone pancreatitis parameters in the ranson criteria at admission?

A
  1. Age > 55 years
  2. White blood cellcount > 16,000 cells/mm3
  3. Blood glucose> 200 mg/dL
  4. SerumAST> 250 IU/L
  5. SerumLDH> 350 IU/L
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10
Q

What are the non-gallstone pancreatitis parameters in the ranson criteria w/in 48 hrs?

A
  1. Serum calcium < 8.0 mg/dL
  2. Hctfall > 10%
  3. PaO2< 60 mmHg
  4. BUN↑ by ≥ 5 mg/dL after IV fluid hydration
  5. Base deficit > 4 mEq/L
  6. Sequestration of fluids > 6 L
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11
Q

What are the gallstone pancreatitis parameters in the ranson criteria at admission?

A
  1. Age in years > 70 years
  2. White blood cell count > 18,000 cells/mm3
  3. Serum glucose> 220 mg/dL
  4. SerumAST> 250 IU/L
  5. SerumLDH > 400 IU/L
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12
Q

What are the gallstone pancreatitis parameters in the ranson criteria w/in 48 hrs?

A
  1. Serum calcium < 8.0 mg/dL
  2. Hct fall > 10%
  3. PaO2< 60 mmHg
  4. BUN↑ by ≥ 2 or more mg/dL after IV fluid hydration
  5. Base deficit > 5 mEq/L
  6. Sequestration of fluids > 4 L
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13
Q

What are the scores for the ranson criteria and what do they correlate with?

A
  1. ≥ 3 = acute severe pancreatitis
  2. < 3 = acute mild pancreatitis
  3. 0-2 points: Mortality = 1%
  4. 3-4 points: Mortality = 16%
  5. 5-6 points: Mortality = 40%
  6. 7-11 points: Mortality ≈100%
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14
Q

What is the PANCREAS acronym for the glasgow prognosis score?

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

When is the APACHE III score used?

A
  1. ICU admission score only
    A. Not pancreatitis specific
    B. Not recalculated during hospitalization
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16
Q

How is APACHE III calculated?

A 
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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17
Q

What is the rx for 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 (total peripheral nutrition) to reverse the catabolic state
    F. PPI to↓ gastric acid production
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18
Q

what are acute pancratitis pts monitored for?

A 
1. Pancreatic pseudocyst
→ infection, hemorrhage, obstruction & rupture
2. Renal failure 
3. Pleural effusion
4. Hypocalcemia
5. Pancreatic abscess
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19
Q

What is a pancreatic pseudocyst?

A

Circumscribed collection of fluid rich inpancreatic enzymes,blood, &necrotic tissue

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20
Q

What is chronic pancreatitis? What can it cause?

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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21
Q

What ppl is chronic pancreatitis more common in?

A
  1. M > F (5:1)

2. Most common start at 30–40 yr

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22
Q

What is the most common cause of acute pancreatitis? What is the pathophys?

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
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23
Q

What are non ETOH causes of chronic pancreatitis?

A
  1. Cholelithiasis
  2. PUD
  3. Hyperparathyroidism/Hypercalcemia
  4. Hyperlipidemia/Hypertriglyceridemia
    ERCP
  5. Hereditary disorders (Cystic Fibrosis)
  6. Smoking ↑ risk w/ ETOH abuse
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24
Q

What is the classic triad of causes of chronic pancreatitis?

A
  1. Classic triad (20% of cases)
    A. Pancreatic calcification
    B. Steatorrhea
    C. DM
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25
Q

What are the sxs of 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
9. pallor, jaundice
10. Rarely, a tender fullness or mass may be palpated in epigastrium
26
Q

What are the dx studies for chronic pancreatitis?

A
  1. Lab testing – most helpful during acute or advanced disease
  2. ↑ Alk phos/bilirubin if significant duct obstruction
  3. Serum amylase & lipase – normal to slightly ↑
  4. Serum Trypsin <10 ng/mL in advanced Dz
  5. Secretin-Caerulein test (SCT)
    A. Gold Standard for pancreatic function
  6. Fecal testing
    A. Quantitative fecal fat
    B. Chymotrypsin
    C. Pancreatic elastase 1
27
Q

What is the secretin-caerulein test?

A
  1. Combination of caerulein & secretin bolus given via gastrofiberscope
  2. Stimulate pancreatic exocrine secretion
  3. Measurement of duodenal juice
  4. Safe, reliable, & effective mean for the purpose of testing pancreatic function
28
Q

What imaging is used to evaulate pancreatic calcification in chronic pancreatitis?

A
  1. Ultrasound (Endoscopic USN prn)
  2. CT scan
  3. ERCP (most sensitive)
  4. MRCP
29
Q

What is the rx for chronic pancreatitis?

A

1.May require hospitalization:
A. Pain management
B. IV hydration
C. Nutritional support – NG tube feedings may be necessary for several weeks for weight loss
D. Synthetic pancreatic enzymes
-Taken w/ every meal to help food digestion & regain weight

30
Q

How is chronic pancreatitis managed long term?

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
    A. Insulin for DM
31
Q

What are the potential complications of 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
    A. 4% after 20 yr of Dz
    B. 19% after age 50
32
Q

What is pancreatic insufficiency/malabsorption?

A
  1. Inadequate metabolism of dietary substances due to defects in digestion, absorption, or transport
  2. Interferes w/ nutrient absorption in small intestine
  3. Results from mucosal disruption caused by
    A. Gastric or intestinal resection
    B. Vascular disorders
    C. Intestinal Dz
    D. Pancreatic insufficiency
33
Q

What can cause pancreatic insufficiency?

A
  1. Chronic pancreatitis
  2. Pancreatic carcinoma
  3. Pancreatic resection
  4. Cystic Fibrosis

Significant damage to or loss of pancreatic tissue required to cause malabsorption
Pancreas secretes ≈ 2L of pancreatic juice qd
Water, bicarbonate, & enzymes to digest fats, proteins, carbohydrates
Insufficient amount of 1 or all

34
Q

What is the chief problem in pancreatic insufficiency?

A

Fat maldigestion -chief problem

Malnutrition & weight loss are also common

35
Q

How does an acidic pH increase malabsorption?

A
  1. Absence of pancreatic bicarbonate in duodenum & jejunum causes acidic pH
  2. ↑ maldigestion by
  3. Precipitates bile salts & prevents activation of the pancreatic enzymes
36
Q

How is pancreatic insufficiency dxed?

A
  1. Diagnosis made by pancreatic function testing (PFT)
    A. Fecal fat
    B. Fecal elastase
    C. Secretin-caerulein test (SCT) : Gold standard
37
Q

How is pancreatic insufficiency managed?

A

Management includes enzyme replacement & fat soluble vitamin therapy

38
Q

What are the epidemiologic trends n pancreatic cancer?

A
  1. 4th leading cause of death
  2. M > F
  3. Median survival is 12-24 months
39
Q

What type of pancreatic cancer is most common?

A

Adenocarcinoma accounts for 90% of pancreatic tumors

40
Q

What are the risk factors for pancreatic cancer?

A
  1. ETOH abuse
  2. Tobacco use
  3. Increased age
  4. Obesity
  5. Long standing Hx of DM (1° in women)
  6. Chronic pancreatitis
  7. Heredity
41
Q

What are the sxs of pancreatic cancer?

A
  1. Painless jaundice
  2. Epigastric pain
  3. Weight loss
  4. Anorexia
  5. Pruritus
  6. Nausea/Vomiting
  7. Palpable liver
  8. Clay colored stools
  9. Courvoisier’s Sign
    A. Nontender, enlarged GB w/ jaundice
  10. Trousseau Sign
  11. Virchow’s Node
  12. Blumer’s Shelf: palpable mass in rectal pouch
  13. Sister Mary Joseph Nodule
42
Q

What are the dx studies for pancreatic cancer?

A
  1. CT , MRI, USN, ERCP, MRCP, PET scan
  2. CBC
  3. CMP (Alk Phos, GGT,AST, ALT)
  4. Amylase, Lipase
  5. CA 19-9 antigen to follow (not for screening)
    CEA
43
Q

What is the tx for pancreatic cancer?

A
  1. Whipple Procedure (surgery)
  2. Surgery + chemotherapy & external beam radiation
    A. 40% 2-yr survival
    B. 25% 5-yr survival
    3.Symptomatic treatment
44
Q

What factors define inoperability in pancreatic cancer?

A
  1. Vascular encasement
  2. Liver Mets
  3. Peritoneal implants
  4. Distal lymph node mets
45
Q

When is combination surgery and chemo used for pancreatic cancer?

A

Combination Tx used for localized but unresectable tumors & results in median survival ≈ 1 yr

46
Q

What is the symptomatic treatment for pancreatic cancer?

A
  1. End of Life Discussion/Hospice
  2. Moderate to Severe Pain
    A. Opioids
    B. Percutaneous or operative splanchnic (celiac) block
47
Q

What is the prognosis for pancreatic cancer?

A
  1. Prognosis varies w/ stage but overall is poor
    A. 5-yr survival < 2%
    B. Due to advanced Dz at diagnosis
48
Q

What is the most important fact about pancreatic cancer?

A

Painless jaundice is Pancreatic Cancer until proven otherwise!

49
Q

What is an insulinoma?

A

Rare pancreatic beta cell tumor that hypersecretes insulin (Hyperinsulinism)

50
Q

What is Whipple’s triad and when is it used?

A
  1. Insulinoma
    A. Low serum glucose (<50 mg/dL)
    B. CNS symptoms of hypoglycemia
    C. Eating carbohydrates relieves symptoms
51
Q

What is the treatment of insulinoma?

A

Surgical resection

52
Q

What are Gastrinomas (AKA Zollinger-Ellison Syndrome)?

A
  1. Z-E syndrome caused by a gastrin-producing tumor usually located in the pancreas, duodenal wall, or lymph nodes
  2. Gastric acid hypersecretion by parietal cells & gastric/peptic ulcerations result
53
Q

What are the sxs of gastrinomas?

A

pain, chronic diarrhea, steatorrhea, weight loss, hematemesis

54
Q

What are the dx studies for gastrinomas?

A

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

55
Q

What is the treatment for gastrinomas?

A

PPI & surgical resection

56
Q

What is a vipoma?

A
  1. Malignant pancreatic islet cell tumor secreting vasoactive intestinal peptide (VIP)→
    A. Syndrome of extreme Watery Diarrhea, Hypokalemia, and Achlorhydria* (WDHA syndrome)
    B. *Production of gastric acid in the stomach is absent or low
57
Q

How are vipomas dxed?

A
  1. serum VIP levels

2. Tumor is localized w/ CT & endoscopic USN

58
Q

How are vipomas treated?

A

Surgical resection

59
Q

What is a glucagonoma?

A

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

60
Q

What are the sxs of glucagonoma?

A
  1. Causes hyperglycemia & characteristic skin rash
  2. Found on shin, face, & groin
  3. Necrolytic migratory erythema
61
Q

How are glucagonomas dxed?

A
  1. Diagnosis is by ↑ glucagon levels & imaging studies

2. Tumor localized w/ CT & endoscopic USN

62
Q

How are glucogonomas treated?

A

Surgical resection

Gen Med: GI (16 decks)

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