Study Points

Pancreatic Cancer

Course #90240 - $60 • 10 Hours/Credits

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  • Participation Instructions
    • Review the course material online or in print.
    • Complete the course evaluation.
    • Review your Transcript to view and print your Certificate of Completion. Your date of completion will be the date (Pacific Time) the course was electronically submitted for credit, with no exceptions. Partial credit is not available.
  1. The median age at diagnosis of pancreatic cancer is

    EPIDEMIOLOGY

    During 2021 in the United States, an estimated 60,430 people will be diagnosed with pancreatic cancer, which represents 3.2% of all new cancer cases and the 11th most common new cancer diagnosis. The median age at diagnosis is 70 years [18].

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  2. Which of the following statements regarding diet and pancreatic cancer risk is FALSE?

    EPIDEMIOLOGY

    There is some evidence that higher consumption of red/processed meat is associated with elevation in pancreatic cancer risk, but other studies have failed to identify dietary risk factors for PDAC [11]. Pancreatic cancer incidence may be lower in persons with higher intake of fresh fruits and vegetables rich in folate and lycopenes (e.g., tomatoes) [30].

    A link between vitamin D and risk for pancreatic cancer is inconsistent, but some data suggest low plasma 25-hydroxyvitamin D levels may increase the risk for pancreatic cancer, especially in those with low retinol/vitamin A intake [31]. Coffee and tea consumption are not associated with pancreatic cancer risk, despite early reports to the contrary [24].

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  3. Starting at 30 months prediagnosis, pancreatic ductal adenocarcinoma (PDAC) showed three distinct metabolic phases. Which of the following is NOT one of these phases?

    EPIDEMIOLOGY

    Numerous studies have identified new-onset diabetes, weight loss, and soft tissue changes in patients with PDAC at diagnosis, but their inter-relationship and connection to PDAC remained unaddressed. From 2000 through 2015, temporal changes in the five years preceding PDAC diagnosis of 219 patients diagnosed with PDAC were compared to 657 controls [46]. From 60 to 30 months before PDAC diagnosis, patients did not significantly differ from controls. However, starting at 30 months prediagnosis, PDAC showed three distinct metabolic phases, each marked by onset and significant progressive worsening of one or more metabolic abnormalities [46]:

    • Phase 1, hyperglycemia (30 to 18 months before PDAC diagnosis): A significant proportion of patients develop hyperglycemia, without soft tissue changes.

    • Phase 2, pre-cachexia (18 to 6 months before PDAC diagnosis): Decreases in serum lipids, weight loss, and the first soft tissue change (subcutaneous abdominal tissue loss) are seen. A profile appears of advanced prediabetes (i.e., fasting blood glucose 120–126 mg/dL or A1c of 6% to 6.5%). In type 2 diabetes, this is associated with weight gain and hyperlipidemia due to insulin resistance. In PDAC, decreases in weight and serum lipids despite rising glucose levels are paradoxical.

    • Phase 3, cachexia (less than 6 months before PDAC diagnosis): Onset of muscle loss, visceral adipose tissue loss, and decreasing high-density lipoprotein. Continued decreases in all other serum lipids, subcutaneous abdominal tissue, and weight. Fasting blood glucose continues rising.

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  4. The most common precancerous precursor lesions associated with pancreatic cancer are

    PATHOPHYSIOLOGY

    Through pathways and somatic mutations that differ modestly in each lesion, PDAC develops from precancerous precursor lesions: pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasm (IPMN), and mucinous cystic neoplasms (MCNs). The most common are PanINs (approximately 90%), and the least common are MCNs. However, all precursor lesions have key similarities [4,48,50]:

    • Early oncogene mutations initiate tumorigenesis.

    • Later loss of tumor suppressor genes drive tumor progression, high-grade dysplasia, and invasive cancer.

    • Increasing grades of dysplasia are associated with accumulation of somatic mutations in key driver genes.

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  5. Which of the following statements regarding pancreatic cancer screening is TRUE?

    PANCREATIC CANCER SCREENING

    With the low population incidence of PDAC (lifetime risk: 1.3%), absence of biomarker screening targets, and high cost of sensitive imaging methods, the U.S. Preventive Services Task Force recommended against screening for pancreatic cancer in asymptomatic adults in 2019, reaffirming its previous conclusion in 2004 [74]. As population screening to achieve earlier detection and intervention of PDAC is not currently feasible, other approaches for this objective have been identified.

    In Australia, public awareness campaigns have highlighted the often vague symptoms of PDAC and encouraged individuals to seek medical attention early. Underscoring this point, one study found that many people who were ultimately diagnosed with PDAC were falsely reassured by the subtle, intermittent nature of their symptoms over the preceding months [75,76].

    As a relatively rare cancer, many primary care providers will only see a PDAC case every few years, making it imperative to elevate awareness of early PDAC signs and symptoms among these professionals. A retrospective case-control study in primary care found that patients sought medical attention 18 times on average in the period preceding their pancreatic cancer diagnosis. PDAC was associated with 11 alarm symptoms; back pain, lethargy, and new-onset diabetes were unique features of PDAC [75,77].

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  6. Most pancreatic cancers (approximately 75%) originate in the

    CLINICAL EVALUATION OF PANCREATIC CANCER

    Most pancreatic cancers (approximately 75%) originate in the head of the pancreas and typically metastasize to regional lymph nodes first, then to the liver. PDAC can also directly invade surrounding visceral organs (e.g., duodenum, stomach, colon); metastasize to any surface in the abdominal cavity via peritoneal spread where development of ascites carries an ominous prognosis; or spread to the skin as painful nodular metastases. By the time of diagnosis, 85% to 90% of patients have locally advanced tumors that have involved retroperitoneal structures, spread to regional lymph nodes, or metastasized to the liver or lung [2,13,24,81].

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  7. Which of the following should trigger inclusion of PDAC in the differential diagnosis?

    CLINICAL EVALUATION OF PANCREATIC CANCER

    Development of abdominal pain, jaundice, or weight loss in the context of newly diagnosed diabetes, family history of PDAC, or history of pancreatitis should trigger inclusion of PDAC in the differential diagnosis [2]. Furthermore, past three-year onset of diabetes or ongoing hyperglycemia with significant weight loss and decreasing serum lipids should be considered a potential PDAC, even if abdominal pain or jaundice are absent, with urgent referral a priority.

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  8. Referral for genetic counseling should be considered for patients diagnosed with pancreatic cancer, especially those

    CLINICAL EVALUATION OF PANCREATIC CANCER

    Referral for genetic counseling should be considered for patients diagnosed with pancreatic cancer, especially those with a family history of cancer or who are young, those of Ashkenazi Jewish ancestry, or for whom a hereditary cancer syndrome is suspect. A free pancreatic cancer risk prediction tool, PancPRO, is available and may help determine risk [11].

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  9. Which of the following is the most common sign/symptom in patients with pancreatic cancer?

    CLINICAL EVALUATION OF PANCREATIC CANCER

    Abdominal pain is the most common symptom, usually insidious in onset and often present for one to two months at the time of presentation, the pain is often severe, and unrelenting in nature. The typical gnawing, visceral quality of pain is generally epigastric, radiating to the sides and/or straight through to the back; some patients may describe the pain as originating in the back. Nighttime pain is often the predominant complaint. Some patients note increased pain after eating and worsened pain when lying flat [24,81]. Rarely, acute pain develops when an episode of acute pancreatitis results in tumor occlusion of the main pancreatic duct [84].

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  10. Which of the following is a common site of metastases in patients with advanced pancreatic cancer?

    CLINICAL EVALUATION OF PANCREATIC CANCER

    Metastatic disease most commonly affects the liver, peritoneum, lungs, and less frequently, bone [24,84]. Patients presenting with or developing advanced intra-abdominal disease may have ascites, a palpable abdominal mass, hepatomegaly from liver metastases, or splenomegaly from portal vein obstruction. Subcutaneous metastases (termed Sister Mary Joseph nodules) in the paraumbilical area signify advanced disease; pancreatic cancer is the origin of a cutaneous metastasis to the umbilicus in 7% to 9% of cases [24,84]. A metastatic mass in the rectal pouch may be palpable on rectal examination (Blumer shelf). As a metastatic node, left supraclavicular lymphadenopathy may be palpable, while other nodes in the cervical area may also be involved.

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  11. What is the preferred imaging for initial evaluation of suspected PDAC?

    THE DIAGNOSTIC AND STAGING WORKUP

    Multidetector computed tomography (MDCT) angiography with intravenous (IV) contrast is the preferred imaging for initial evaluation of suspected PDAC. The Pancreatic CT Protocol standardizes its use, making MDCT highly accurate for assessing tumor extent, vascular invasion, and distant metastases [11,16,88,89]. The NCCN recommends that MDCT angiography should also cover the chest and pelvis for complete staging [11].

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  12. Although unsuitable for asymptomatic screening, which biomarker is the most clinically useful in PDAC?

    THE DIAGNOSTIC AND STAGING WORKUP

    CA19-9 is a sialylated Lewis A blood group antigen, commonly expressed and shed in benign and malignant pancreatic and biliary disease. Although unsuitable for asymptomatic screening, CA19-9 is the most clinically useful biomarker in PDAC, with good sensitivity (79% to 81%) and specificity (82% to 90%) in symptomatic patients. A normal serum level is 37 U/mL [90].

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  13. According to the NCCN guideline, PDAC tumors that are involved with nearby structures would be classed as

    THE DIAGNOSTIC AND STAGING WORKUP

    The NCCN guideline classes PDAC resectability into the following clinical stages [11]:

    • Stage 1: Resectable

    • Stage 2: Borderline resectable (i.e., tumors that are involved with nearby structures so as to be neither clearly resectable nor clearly unresectable with a high chance of removal of all macroscopic disease)

    • Stage 3: Locally advanced (i.e., tumors that are involved with nearby structures to an extent that renders them unresectable despite the absence of metastatic disease)

    • Stage 4: Metastatic (i.e., non-resectable)

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  14. A patient with pancreatic cancer who is capable of all self-care but unable to carry out any work activities would receive an Eastern Cooperative Oncology Group Performance Status (ECOG) score of

    TREATMENT APPROACHES FOR PANCREATIC CANCER

    EASTERN COOPERATIVE ONCOLOGY GROUP (ECOG) PERFORMANCE STATUS SCALE

    Score Definition
    0
    Fully active
    No performance restrictions
    1
    Strenuous physical activity restricted
    Fully ambulatory and able to carry out light work
    2
    Capable of all self-care but unable to carry out any work activities
    Up and about >50% of waking hours
    3
    Capable of only limited self-care
    Confined to bed or chair >50% of waking hours
    4
    Completely disabled
    Cannot carry out any self-care
    Totally confined to bed or chair
    5Deceased
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  15. The conventional Whipple procedure (pancreaticoduodenectomy) is used for tumors

    TREATMENT APPROACHES FOR PANCREATIC CANCER

    Used for tumors in the pancreatic head or periampullary region, the conventional Whipple procedure involves removal of the pancreatic head, duodenum, gallbladder, and the antrum of the stomach, with surgical drainage of the distal pancreatic duct and biliary system, usually through anastomosis to the jejunum. The primary reason for removing so much of the intra-abdominal structures is that they all share a common blood supply [24,102].

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  16. Which chemotherapy agent/regimen has the strongest recommendation and level of evidence for use in patients with stage 3 (locally advanced) PDAC?

    TREATMENT APPROACHES FOR PANCREATIC CANCER

    NCCN TREATMENT SUMMARY FOR PDAC

    Strength of Recommendation/EvidenceRegimenNotesa
    Adjuvant stage 1 (resectable)
    Category 1
    Gemcitabine
    Gemcitabine/capecitabine
    5-FU/leucovorin
    Category 2a
    5-FU continuous infusion
    Chemoradiation
    Chemoradiation should follow induction chemotherapy, with or without subsequent chemotherapy
    Category 2BCapecitabine
    Neoadjuvant stage 1/2 (resectable or borderline resectable)
    Category 2AGemcitabine/paclitaxel NAB
    Category 2B
    Gemcitabine/cisplatinb
    FOLFIRINOX
    Chemoradiation
    Stage 3 (locally advanced)
    Category 1GemcitabinePreferred for patients with poor ECOG PS (≥2)
    Category 2A
    Gemcitabine/paclitaxel NAB
    Gemcitabine/erlotinib
    Gemcitabine/cisplatinb
    Gemcitabine/capecitabine
    Gemcitabine fixed-dose rate
    FOLFIRINOX
    Chemoradiation
    Fixed-dose rate gemcitabine is a category 2B recommendation for patients with poor ECOG PS (≥2)
    Chemoradiation should follow induction chemotherapy, with or without subsequent chemotherapy
    Category 2B
    Gemcitabine/docetaxel/capecitabine Capecitabine
    5-FU continuous infusion
    FOLFOX
    Stage 4 (metastatic)
    Category 1
    Gemcitabine
    Gemcitabine/paclitaxel NAB (preferred)
    Gemcitabine/erlotinib
    FOLFIRINOX (preferred)
    Category 2A
    Gemcitabine/cisplatinb
    Gemcitabine/capecitabine
    Gemcitabine fixed-dose rate
    Olaparib
    Pembrolizumab (for MSI-H or dMMR tumors only)
    Larotrectinib (for NTRK-positive only)
    Fixed-dose rate gemcitabine is a category 2B recommendation for patients with poor ECOG PS (≥2)
    Olaparib for maintenance therapy only in BRCA1/2 or PALB2 mutated stage 4 disease without progression after 4 to 6 months of first-line platinum-based therapy
    Category 2B
    Gemcitabine/docetaxel/capecitabine
    Capecitabinec
    5-FU continuous infusionc
    FOLFOX
    Entrectinib (for NTRK-positive only)
    Second-line therapy
    Category 1
    Gemcitabinec,d
    5-FU/leucovorin/irinotecand
    Category 2AGemcitabine fixed-dose rateFixed-dose rate gemcitabine is a category 2B recommendation for patients with poor ECOG PS (≥2)
    Category 2B
    Capecitabinec,e
    5-FU continuous infusionc,e
    Strength of Recommendation Definitions
    CategoryDefinition
    1Based upon high-level evidence, there is uniform NCCN consensus that the intervention is appropriate.
    2ABased upon lower-level evidence, there is uniform NCCN consensus that the intervention is appropriate.
    2BBased upon lower-level evidence, there is NCCN consensus that the intervention is appropriate.
    aECOG performance status (PS) 0/1 only, unless noted.
    bIn BRCA1/2 or PALB2 mutations only.
    cPoor ECOG PS (≥2) only.
    dIf prior non-gemcitabine-based therapy.
    eIf prior gemcitabine-based therapy.
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  17. ASTRO guidelines for neoadjuvant chemoradiation specify a radiation dose of

    TREATMENT APPROACHES FOR PANCREATIC CANCER

    ASTRO guidelines for neoadjuvant chemoradiation specify a radiation dose of 4,500–5,040 cGy in 180–200 cGy fractions [12]. They recommend delivery of radiation therapy following two to six months of chemotherapy.

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  18. To address bile duct obstruction in patients with PDAC, the preferred approach is

    PALLIATION AND SYMPTOMATIC MANAGEMENT

    Endoscopic retrograde stenting is superior to surgical or percutaneous approaches to address bile duct obstruction because of a more favorable adverse event rate. Self-expandable metal stents are preferred over plastic stents in patients with a life expectancy of more than three months in terms of patency duration, less therapeutic failure and need for reintervention, lower cholangitis incidence, and better patient quality of life. Patency rates between covered and uncovered metal stents are not significantly different [16]. Endoscopic ultrasonography-guided biliary drainage is an alternative if endoscopic biliary stent placement is unsuccessful or technically not feasible.

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  19. Which agents have proven efficacy in the treatment of anorexia associated with cancer-related anorexia/cachexia syndrome?

    PALLIATION AND SYMPTOMATIC MANAGEMENT

    Many agents have been evaluated for the treatment of CACS, but only corticosteroids (e.g., dexamethasone) and progesterone analogs (e.g., megestrol acetate) have a proven benefit in the anorexia associated with this syndrome [122]. Selection is based on life expectancy and assessment of risks versus benefits. Dexamethasone is suggested for patients for whom only weeks of therapy are anticipated, while megestrol acetate or medroxyprogesterone acetate (another progesterone analog) are suggested for patients with longer life expectancies [126].

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  20. When providing education to caregivers of patients with PDAC, which of the following points related to nutrition should be emphasized?

    PALLIATION AND SYMPTOMATIC MANAGEMENT

    Family members in particular can require educational intervention, as their distress may manifest in attempts to pressure or coerce the patient into increased feeding. Key points to discuss with patients and their family members, related to interactions about nutrition and eating near the end of life, include the following [131]:

    • Loss of appetite is common in patients with advanced cancer and may be the result of the cancer process itself.

    • Trying to force a patient to eat is usually counterproductive, potentially leading to increased nausea/vomiting.

    • In most patients with advanced cancer and cachexia, providing additional calories by feeding tubes and/or intravenously does not improve outcomes.

    • Trying to make a patient eat, when they have marked appetite loss, can lead to decreased social interactions and increased patient distress regarding interactions with caregivers (including stories of patients, in their dying days, pretending to be asleep when relatives visit, so that the relatives do not try to make them eat something).

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  • Back to Course Home
  • Participation Instructions
    • Review the course material online or in print.
    • Complete the course evaluation.
    • Review your Transcript to view and print your Certificate of Completion. Your date of completion will be the date (Pacific Time) the course was electronically submitted for credit, with no exceptions. Partial credit is not available.