Posted on by Joel Topf

AI Curriculum

I am still in the “amazed by what AI can do” stage

Here is me prompt

i am teaching a class on electrolyte abnormalities for nephrologists. What would be good tricky things to teach

I then ran my prompt through an AI to make my prompt “better” This AI is called PromptPerfect. Here is what it came up with:

As part of my curriculum for a class aimed at nephrologists focusing on electrolyte abnormalities, I am seeking innovative and challenging concepts that can enhance the learning experience. The goal is to identify complex scenarios or case studies that delve into the nuances of electrolyte homeostasis, including mechanisms, clinical implications, and diagnostic challenges. I would appreciate suggestions for specific topics that could provoke critical thinking and discussion among the attendees, such as rare electrolyte disorders, atypical presentations, or the interplay between various electrolytes in different clinical contexts. Additionally, please provide a structured outline of how these concepts can be presented, including key points, potential teaching methods, and examples that could facilitate understanding.

And here is the output that Chat GPT4o came up with:

Electrolyte curriculum for nephrologists.docDownload

Curriculum Outline: Innovative and Challenging Electrolyte Abnormalities for Nephrologists

Module 1: Rare Electrolyte Disorders – Uncommon Mechanisms and Diagnosis

Key Concept: Understanding rare electrolyte disturbances that involve complex mechanisms and atypical presentations.

Key Topics to Discuss:

  1. Hyperkalemic Periodic Paralysis (HPP)
    • Mechanism: Mutations in the sodium channel (SCN4A), leading to abnormal potassium shifts during exercise or fasting.
    • Clinical Implication: Presentation with episodic muscle weakness and hyperkalemia.
    • Diagnostic Challenge: Distinguishing HPP from other causes of hyperkalemia, such as renal failure or medications.
    • Teaching Method:
      • Interactive Case Discussion: Present a case of a young athlete with recurrent episodes of weakness and hyperkalemia. Explore diagnostic tests (genetic testing, muscle biopsy).
      • Group Activity: Have the class brainstorm possible causes of episodic hyperkalemia and narrow down to rare causes like HPP.
  2. Familial Hyperkalemic Hypertension (FHHt)
    • Mechanism: Mutations in the WNK1 and WNK4 genes leading to excessive sodium retention and secondary hyperkalemia.
    • Clinical Implication: Hypertension with normal or elevated potassium despite low renin and aldosterone.
    • Diagnostic Challenge: Differentiating FHHt from primary hyperaldosteronism or renovascular hypertension.
    • Teaching Method:
      • Case Study: Present a hypertensive patient with hyperkalemia, and have learners differentiate between FHHt and other causes of secondary hypertension.
      • Interactive Q&A: Ask the learners to discuss how genetic testing can be used for diagnosis, and compare the pathophysiology with other causes of secondary hypertension.
  3. Tumor Lysis Syndrome (TLS) and Electrolyte Imbalances
    • Mechanism: Rapid release of intracellular electrolytes (potassium, phosphate, and uric acid) due to tumor cell lysis.
    • Clinical Implication: TLS can cause hyperkalemia, hyperphosphatemia, and hypocalcemia, along with acute kidney injury (AKI).
    • Diagnostic Challenge: Early detection of TLS in the absence of clinical symptoms; managing high-risk patients pre-emptively.
    • Teaching Method:
      • Case Study: Present a cancer patient undergoing chemotherapy with electrolyte abnormalities and acute kidney injury. Discuss management strategies, including allopurinol, rasburicase, and hydration.
      • Interactive Poll: Ask learners how they would manage a patient at risk of TLS in the first 48 hours.

Module 2: Electrolyte Imbalance in Multi-System Disease

Key Concept: The interplay between various electrolytes in patients with complex co-morbidities and multi-system disease.

Key Topics to Discuss:

  1. Hyponatremia in Heart Failure and Cirrhosis
    • Mechanism: Discuss hypervolemic hyponatremia in the context of heart failure (low cardiac output, increased ADH release) and cirrhosis (portal hypertension, ascites, altered renal perfusion).
    • Clinical Implication: Both conditions may result in SIADH-like patterns with hypovolemic and euvolemic hyponatremia.
    • Diagnostic Challenge: Distinguishing between cirrhosis with ascites and heart failure with ascites as causes of hyponatremia.
    • Teaching Method:
      • Case Comparison: Present two cases of hyponatremia—one in a patient with heart failure and the other with cirrhosis—and have learners compare and contrast their approaches to diagnosis and management.
      • Group Discussion: Have attendees discuss the pathophysiology of hepatorenal syndromeand cardiorenal syndrome as part of electrolyte disturbances.
  2. Potassium Abnormalities in Diabetic Ketoacidosis (DKA)
    • Mechanism: Insulin deficiency, acidosis, and shifts in potassium from the intracellular to extracellular space in DKA.
    • Clinical Implication: Potassium levels can be falsely elevated on presentation due to transcellular shifts, and may drop quickly with insulin therapy.
    • Diagnostic Challenge: Assessing potassium levels and deciding when and how to replete potassium during DKA treatment.
    • Teaching Method:
      • Interactive Case Discussion: Present a case of a diabetic patient with hyperkalemia and acidosis. Discuss the initial approach to potassium monitoring and replacement during DKA management.
      • Problem-Solving Exercise: Have learners calculate the correct amount of potassium to replete in DKA while managing acid-base status and avoiding hypokalemia.

Module 3: Complex Electrolyte Interactions and Their Clinical Impact

Key Concept: Understanding the dynamic interplay between multiple electrolytes in clinical scenarios, and how changes in one can impact others.

Key Topics to Discuss:

  1. The Calcium-Phosphate Paradox in Chronic Kidney Disease
    • Mechanism: In CKD, impaired phosphate excretion leads to elevated phosphate levels, which bind to calcium and precipitate in tissues, contributing to vascular calcification and secondary hyperparathyroidism.
    • Clinical Implication: Elevated calcium-phosphate product is a risk factor for cardiovascular morbidity.
    • Diagnostic Challenge: Monitoring and managing the calcium-phosphate product in the context of dialysis or advanced CKD.
    • Teaching Method:
      • Interactive Discussion: Present a dialysis patient with elevated calcium, phosphate, and secondary hyperparathyroidism. Have learners propose management strategies to reduce the calcium-phosphate product.
      • Case Study: Explore the role of calcimimetics, phosphate binders, and vitamin D analogs in controlling the calcium-phosphate product.
  2. Magnesium and Potassium Imbalances: The Subtle Interplay
    • Mechanism: Hypomagnesemia often accompanies hypokalemia, and correcting hypokalemia without addressing magnesium deficiency can lead to refractory hypokalemia.
    • Clinical Implication: Magnesium plays a crucial role in potassium regulation, and untreated magnesium deficiency can hinder recovery of normal potassium levels.
    • Diagnostic Challenge: Identifying hypomagnesemia in patients with unexplained hypokalemia.
    • Teaching Method:
      • Case Presentation: Present a patient with refractory hypokalemia that doesn’t improve despite treatment. Lead a discussion on the potential underlying magnesium deficiency and the rationale for magnesium repletion.
      • Interactive Exercise: Have learners analyze lab results and decide whether magnesium levels should be checked in cases of hypokalemia.
  3. Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors and Electrolyte Shifts
    • Mechanism: SGLT2 inhibitors, used in diabetes and CKD, can cause increased sodium excretion, leading to fluid shifts and electrolyte disturbances (e.g., hyponatremia, hypokalemia).
    • Clinical Implication: The risk of electrolyte abnormalities is increased with dehydration,diuretics, or acute kidney injury in patients on SGLT2 inhibitors.
    • Diagnostic Challenge: Early identification of electrolyte imbalances when patients are on SGLT2 inhibitors, especially during periods of acute illness or volume depletion.
    • Teaching Method:
      • Case Study: Present a patient on SGLT2 inhibitors who presents with confusion and low sodium. Discuss the role of SGLT2 inhibitors in electrolyte homeostasis and how to adjust treatment when using these drugs.
      • Interactive Poll: Ask learners to suggest steps for managing a patient on SGLT2 inhibitors who presents with dehydration and electrolyte abnormalities.

Teaching Methods and Approaches

  1. Case-Based Learning: Provide complex, real-world cases where the students can apply their knowledge of electrolyte abnormalities in clinical scenarios. Case discussions should prompt learners to think critically about diagnosis, pathophysiology, and management.
  2. Small Group Discussions: Break learners into smaller groups to tackle specific topics or case studies. Afterward, have each group present their findings and management approach to the class.
  3. Interactive Polls and Quizzes: Use technology (e.g., Kahoot, Mentimeter) to ask clinical questions and prompt learners to choose the best answer. This can be used to initiate discussions and clarify concepts.
  4. Role-Playing and Simulations: Use role-playing to simulate difficult clinical situations (e.g., managing a patient with complex electrolyte imbalances during a crisis). Simulations can help learners practice decision-making under pressure.
  5. Expert Panel Discussions: Bring in experts to discuss the nuances of managing rare or complex electrolyte disorders, especially those with genetic or multi-system involvement.

Conclusion

By focusing on rare disorders, complex interactions, and multi-system involvement, you can stimulate deep clinical reasoning and promote active learning. Encourage learners to approach electrolyte abnormalities not only as isolated issues but also as part of a broader clinical context, where underlying mechanisms, patient history, and comorbidities significantly influence diagnosis and management.

There are some significant mistakes. Secondary hyperparathyroidism is associated with low a calcium, not a high calcium. And the SGLT2i section in Module 3 would have to be entirely abandoned. But for ten minutes of just fucking around with Chat GHPT it is pretty complete and looks like it would make for a pretty compelling curriculum.