| Course | DNRS 6501 Advanced Pathophysiology (DNP level) |
|---|---|
| Week | Week 10 |
| Paper type | Case presentation slide deck |
| Length | About 960 words across 10 slides with speaker notes |
| Format | Slide deck with speaker notes, APA 7 |
| School | Walden University |
| Program | Doctor of Nursing Practice (DNP) |
| Updated | October 2026 |
Free sample paper for DNRS 6501 Week 10
Which Failed First in His Pancreas, the Enzymes or the Insulin?
Student Name
College of Nursing, Walden University
DNRS 6501: Advanced Pathophysiology (DNP level)
Instructor Name
Month Day, Year
Slide 1: Which Failed First in His Pancreas, the Enzymes or the Insulin?
A case of recurrent acute pancreatitis, chronic pancreatitis, and diabetes in one man
Presenter name, DNRS 6501
Speaker notes: Today I want to answer one question about one patient: when his pancreas failed, which of its two jobs went first, digestion or glucose control, and why in that order? The answer matters because the order predicts what his diabetes will look like and what to watch for next.
Slide 2: The Patient
Composite man, 52 years old
Heavy alcohol use for 20 years; smokes a pack a day
Three attacks of acute pancreatitis, ages 44 to 48
Constant upper abdominal pain since 48
Greasy, floating stools and weight loss since 50
Diabetes diagnosed at 51; low blood sugar episodes on insulin
Speaker notes: He is a composite built for teaching. The facts I will use are all on this slide. Notice that the digestive symptoms came before the diabetes, and that his diabetes has an odd feature: he goes low easily on modest insulin doses. Hold on to both.
Slide 3: The Timeline
Age 44, 46, 48: acute attacks
Age 48: pain becomes constant; imaging shows calcifications
Age 50: steatorrhea; fecal elastase low
Age 51: HbA1c 8.4%; C-peptide low
Age 52: two hypoglycemic episodes on 18 units of insulin a day
Speaker notes: This slide exists because the argument is about time. Laid out as a line, the sequence is clear: recurrent attacks, then scarring, then loss of digestive function, then loss of glucose control. The next four slides explain why that order is expected rather than coincidental.
Slide 4: Claim 1, Repeated Attacks Set Up Chronic Disease
After a first attack of acute pancreatitis, about 10% progress to chronic pancreatitis
After recurrent attacks, about 36% do
Alcohol and smoking are the largest risk factors
Speaker notes: The first claim is that his chronic disease began with his acute attacks. A meta-analysis of 14 studies found that about 10% of patients progress to chronic pancreatitis after a first attack and about 36% after recurrent attacks, with alcohol and smoking the largest risk factors (Sankaran et al., 2015). He has all three. The mechanistic definition of chronic pancreatitis describes it as a fibro-inflammatory syndrome in people whose response to repeated injury persists and becomes pathologic (Whitcomb et al., 2016). Each attack injured the gland, and in him the repair did not stop.
Slide 5: Claim 2, Acinar Tissue Is Lost First
Acinar cells are the site of injury in each attack
Fibrosis replaces acinar tissue as it heals
Steatorrhea appears only when lipase output falls below about 10% of normal
Speaker notes: The second claim is about which cells go first. The injury in pancreatitis begins in the acinar cells, the enzyme-making cells, and fibrosis replaces them as the gland heals badly. Digestion has a large reserve: in a classic study, malabsorption of fat did not appear until lipase output fell below about 10% of normal (DiMagno et al., 1973). So by the time he had greasy stools at 50, most of his acinar tissue was already gone.
Slide 6: Claim 3, Islets Are Lost Later
Islets are scattered within the acinar tissue
They survive early injury, then are surrounded and destroyed by fibrosis
Diabetes follows exocrine failure, usually by years
Speaker notes: The third claim explains the delay. Islets are embedded in the acinar tissue but are not the primary target of each attack. As fibrosis advances, it surrounds and destroys them, and insulin secretion falls. That is why, in chronic pancreatitis, diabetes usually appears after exocrine insufficiency, as it did in him, a year after his steatorrhea (Hart et al., 2016).
Slide 7: Claim 4, Losing Islets Is Not Only Losing Insulin
Beta cells lost: insulin falls
Alpha cells lost: glucagon response to hypoglycemia falls
Pancreatic polypeptide lost: hepatic insulin sensitivity falls
Result: type 3c diabetes, prone to hypoglycemia
Speaker notes: The fourth claim explains his lows. When fibrosis destroys islets, it takes all their cell types, not only beta cells. Losing alpha cells blunts glucagon release when glucose falls, so his defense against hypoglycemia is weak. This form is called type 3c, or pancreatogenic, diabetes, and brittle glucose control with hypoglycemia is one of its features (Hart et al., 2016). His 18 units of insulin are not a large dose; his missing glucagon is the reason they drop him low.
Slide 8: What Remains Unexplained
Most heavy drinkers never develop chronic pancreatitis
Why did his repair response persist after each attack?
Genetic and environmental modifiers are suspected; not measured in him
Speaker notes: What I cannot explain is why him. Most people who drink heavily never develop chronic pancreatitis. The mechanistic definition points to genetic, environmental, and other risk factors that make the response to injury persist (Whitcomb et al., 2016), but we have no genetic testing for him, and his smoking is only part of the answer. I would like the discussion to start here.
Slide 9: The Answer
The enzymes failed first
Acinar cells were the target; islets were lost later to fibrosis
His diabetes is type 3c, and his hypoglycemia follows from it
Speaker notes: So the answer to the question on the first slide is that the enzymes failed first, because the acinar cells were the target of each attack and digestion has a large reserve that hides the loss for years. The insulin failed later, and it failed along with glucagon, which is why his diabetes behaves the way it does.
Slide 10: References
DiMagno, Go, and Summerskill, 1973
Hart et al., 2016
Sankaran et al., 2015
Whitcomb et al., 2016
Speaker notes: Full references follow in the list. The meta-analysis and the review of type 3c diabetes are the two I would read first.
References
DiMagno, E. P., Go, V. L. W., & Summerskill, W. H. J. (1973). Relations between pancreatic enzyme outputs and malabsorption in severe pancreatic insufficiency. The New England Journal of Medicine, 288(16), 813-815. https://doi.org/10.1056/NEJM197304192881603
Hart, P. A., Bellin, M. D., Andersen, D. K., Bradley, D., Cruz-Monserrate, Z., Forsmark, C. E., Goodarzi, M. O., Habtezion, A., Korc, M., Kudva, Y. C., Pandol, S. J., Yadav, D., & Chari, S. T. (2016). Type 3c (pancreatogenic) diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer. The Lancet Gastroenterology & Hepatology, 1(3), 226-237. https://doi.org/10.1016/S2468-1253(16)30106-6
Sankaran, S. J., Xiao, A. Y., Wu, L. M., Windsor, J. A., Forsmark, C. E., & Petrov, M. S. (2015). Frequency of progression from acute to chronic pancreatitis and risk factors: A meta-analysis. Gastroenterology, 149(6), 1490-1500. https://doi.org/10.1053/j.gastro.2015.07.066
Whitcomb, D. C., Frulloni, L., Garg, P., Greer, J. B., Schneider, A., Yadav, D., & Shimosegawa, T. (2016). Chronic pancreatitis: An international draft consensus proposal for a new mechanistic definition. Pancreatology, 16(2), 218-224. https://doi.org/10.1016/j.pan.2016.02.001
Reading the DNRS 6501 Week 10 instructions
The tenth week commonly asks for a recorded or narrated case presentation that explains a patient's disease course through its pathophysiology. Slide counts are often capped at around ten to fifteen, and speaker notes or narration carry the explanation. You are expected to introduce the case, show the sequence of events, explain the mechanisms behind each stage and finish with a conclusion or teaching point. References belong on the final slide in APA 7. Some sections add a time limit for the recording, usually between eight and fifteen minutes. A deck organized around a question tends to score better than one that walks through the history in date order. Check whether your instructor wants slides alone, notes alone or both submitted.
How this DNRS 6501 Week 10 example is built
Ten slides and a notes page under each. The title slide carries the question the presentation answers rather than the case name, so the audience knows what is at stake before the first finding appears. Two slides present the composite case, one of them a timeline rather than a list, since the interaction being argued is temporal. Four slides carry the argument, each holding one claim and at most six lines of text, with the evidence for that claim living in the notes instead of on the slide. One slide states what remains unexplained. A references slide follows current citation format. The speaker notes read as sentences a person could say, not as a script transcribed from a paper.
Where the marks sit in the DNRS 6501 Week 10 rubric
Slide density is the first thing marked and the easiest to fix. Sections score the argument itself, so a presentation that walks the case chronologically and never states an interaction has delivered a report rather than an analysis. Credit follows the placement of evidence: sources go in the notes and on the final reference slide, and a slide carrying its own bibliography is usually unreadable. Timing is frequently its own criterion, and a set built for twelve minutes that runs nineteen loses points that the content had already earned. The unexplained slide is worth including even under time pressure, because presentations claiming to account for everything invite exactly the question they cannot answer. Recorded delivery is assessed for pace and audibility in most classrooms that require it.
DNRS 6501 Week 10 help: mistakes that cost marks
Presentations lose marks first for crowded slides with whole paragraphs that the speaker then reads aloud. Keep each slide to a claim and a few supporting points, and put the reasoning in the notes. A second common problem is a timeline with no argument attached, which leaves the audience to work out the mechanism. Give every slide after the case a claim in its title. Students also skip the slide on what the case leaves unexplained, though admitting a gap reads as doctoral thinking. Watch timing, as narrated decks often run long. Check that laboratory values on the timeline match those in the notes. Cite images and figures that are not your own. Finish with a clear answer to the question you posed on the first slide.
Get a DNRS 6501 Week 10 example written to your instructions
Forward the presentation prompt, the time limit, whether a recording is required, and any template the classroom provides, and a slide set with speaker notes comes back to you. The first custom one is free and arrives inside 24 to 48 hours. A case from your own service never needs to reach a slide, and none is reconstructed here.
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DNRS 6501 Week 10 questions, answered
How many slides suit a doctoral case presentation?
Ten works for a twelve to fifteen minute limit, which is a common range in doctoral sections though not a published one. Slide count matters less than the ratio of claims to slides. If your prompt sets a time limit and no slide count, budgeting roughly a minute and a half per argument slide keeps the delivery inside it.
Does the case have to be one the presenter cared for?
Not for this. Composites and published cases carry the assignment perfectly well, and the example uses one. Encounters from your own practice are your record and stay there, so nothing about a real person is reassembled into slides at this desk. Where a classroom supplies a case, the presentation is built on that.
Should the speaker notes be full sentences?
Full sentences that sound spoken, yes, particularly where delivery is recorded and graded. Notes written as paragraphs from a paper produce the reading voice that costs presentation points. The example keeps each note under a minute of speech and marks the two places where the presenter pauses for the audience to read a figure.
Where can I find a free DNRS 6501 Week 10 sample paper?
The ten-slide pancreatitis case presentation is laid out on this page with its speaker notes, the four claims and the answer slide, plus margin notes on each design choice.
What question does the DNRS 6501 Week 10 deck ask?
In a man whose recurrent pancreatitis became chronic disease with diabetes, which failed first, enzyme production or insulin production.