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CDE Diabetes

Study Guide: Neuropathy (Chapter 31)

1. Overview & Pathophysiology

Diabetic neuropathy is a heterogeneous group of disorders affecting the somatic and autonomic nervous systems. It is the most common complication of diabetes.

  • Distal Symmetric Polyneuropathy (DSPN): The most common form, typically presenting as a “stocking-glove” sensory loss or pain. It is a major risk factor for foot ulcers and amputation.

  • Risk Factors: The development of neuropathy is multifactorial. Key risk factors include:

    • Elevated blood glucose (A1C).

    • Elevated triglycerides.

    • High Body Mass Index (BMI).

    • Smoking.

    • Hypertension.

2. Screening Protocols

Screening is vital because the early stages of neuropathy are often asymptomatic (loss of sensation).

  • Frequency:

    • Type 1 Diabetes: Start 5 years post-diagnosis, then annually.

    • Type 2 Diabetes: Start at diagnosis, then annually.

  • Method (The “10g Monofilament”):

    • Screening should include testing with a 10g Semmes-Weinstein monofilament to detect Loss of Protective Sensation (LOPS).

    • Other assessments:

      • Vibration (128 Hz tuning fork).

      • Temperature.

      • Pinprick sensation.

      • Proprioception.

3. Management Strategies

Management is divided into prevention/slowing progression and symptom management.

A. Disease Modification (Glycemic Control)

  • Type 1 Diabetes: Intensive glycemic control significantly prevents or delays the development of neuropathy.

  • Type 2 Diabetes: Intensive control reduces the frequency of neuropathy but is less effective than in Type 1.

B. Management of Painful Neuropathy Neuropathic pain can be severe and debilitating (burning, shooting, lancinating). Treatment aims to reduce pain by ~30–50% and improve quality of life/sleep.

  • First-Line Pharmacotherapy:

    • Anticonvulsants: Pregabalin, Gabapentin.

    • Antidepressants (SNRI): Duloxetine, Venlafaxine.

    • Antidepressants (TCA): Amitriptyline, Nortriptyline (use with caution due to anticholinergic side effects).

  • Second-Line:

    • Opioid-like agents (e.g., Tramadol, Tapentadol) may be considered but have higher risk profiles.

5. Diabetes Canada 2018 Clinical Practice Guidelines Recommendations

Key takeaways from the “Recommendations” section (Page S220).

  1. Screening:

    • Type 1: Screen annually starting 5 years post-diagnosis [Grade D, Consensus].

    • Type 2: Screen annually starting at diagnosis [Grade D, Consensus].

  2. Tools: Use the 10g monofilament testing of the dorsal aspect of the great toe.

  3. Glycemic Control: Optimize control to prevent/delay neuropathy in Type 1 [Grade A, Level 1] and Type 2 [Grade B, Level 2].

  4. Pain Management:

    • Examples of agents: Pregabalin, Duloxetine, Gabapentin, Amitriptyline, Venlafaxine [Grade B, Level 2 for most].

    • Opioids (Tapentadol, Tramadol) are second-line [Grade B].

Reference:

Bril V, Breiner A, Perkins BA, Zochodne D. Neuropathy. Canadian Journal of Diabetes. 2018;42:S217-S221. doi:10.1016/j.jcjd.2017.10.028
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CDE Diabetes

Flashcards: Retinopathy (Chapter 30)

Diabetic retinopathy remains the leading cause of new cases of blindness in working-age adults. These flashcards are designed to help pharmacists and healthcare professionals quickly recall the 2018 Clinical Practice Guidelines regarding screening intervals, the “ABC” prevention strategy, and the shift toward newer pharmacological treatments for preserving vision.

Key Topics Covered:

  • Screening Schedules: Memorizing the distinct initiation times for Type 1 diabetes (5 years post-diagnosis) versus Type 2 diabetes (at diagnosis) and follow-up frequencies.

  • Therapeutic Interventions: Identifying anti-VEGF (vascular endothelial growth factor) therapy as the first-line treatment for center-involved diabetic macular edema (DME).

  • The “ABCs” of Prevention: Recalling the role of optimal A1C, Blood pressure, and Cholesterol control—specifically the use of fenofibrate—in slowing disease progression.

  • Pregnancy Risks: Understanding why pregnancy confers a high risk for rapid retinopathy progression and the need for first-trimester screening.

  • Referral Criteria: Knowing when to refer to an ophthalmologist versus when optometric screening is sufficient.

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CDE Diabetes

Practice Exam: Retinopathy (Chapter 30)

Diabetic retinopathy remains the leading cause of new cases of blindness in adults of working age. The 2018 Clinical Practice Guidelines emphasize that with optimal glycemic and blood pressure control, coupled with regular screening and timely treatment, the vast majority of vision loss can be prevented.

This practice exam tests your ability to apply specific screening schedules, recognize the risk factors for progression, and identify the appropriate therapeutic interventions for sight-threatening disease.

Key Concepts Covered in This Exam:

  • Screening Protocols: Mastering the different screening initiation times for Type 1 diabetes (5 years after diagnosis) versus Type 2 diabetes (at diagnosis) and the frequency of follow-up.

  • Risk Reduction: Understanding the evidence behind “ABC” management (A1C, Blood pressure, Cholesterol) and the specific role of fenofibrate in slowing retinopathy progression.

  • Therapeutic Interventions: Identifying anti-VEGF (vascular endothelial growth factor) therapy as the first-line treatment for center-involved diabetic macular edema (DME), replacing standard laser therapy for many patients.

  • Pregnancy Considerations: Recognizing the rapid progression of retinopathy that can occur during pregnancy and the requirement for more frequent ophthalmological assessments.

  • Referral Pathways: Knowing when to refer patients to an optometrist or ophthalmologist and how to interpret screening results to determine follow-up intervals.

1. A 55-year-old patient is newly diagnosed with type 2 diabetes. When should retinopathy screening be initiated?

2. A 28-year-old patient was diagnosed with type 1 diabetes at age 12. When should screening for retinopathy have commenced according to guidelines?

3. Which of the following best describes proliferative diabetic retinopathy?

4. Which cytokine plays a pivotal role in the development of diabetic macular edema?

5. A patient with type 2 diabetes and established mild retinopathy is currently on atorvastatin. Which additional lipid-lowering therapy could be considered to slow retinopathy progression?

6. According to the Eye Diseases Prevalence Research Group, what is the crude prevalence rate of retinopathy in the adult diabetic population?

7. What is considered the gold standard screening method for diabetic retinopathy?

8. A patient with diabetic retinopathy requires ophthalmic surgery. They are currently taking warfarin for a mechanical heart valve. Based on the evidence, should warfarin be stopped?

9. A patient with moderate visual loss from diabetic retinopathy feels discouraged about their quality of life. What referral is recommended?

10. A patient has centre-involving diabetic macular edema. Which treatment is considered first-line therapy?

11. Visual loss from diabetic retinopathy is associated with which of the following?

12. A patient with diabetes and atrial fibrillation requires anticoagulation but is concerned about eye complications. Based on the evidence, what can you advise about ASA use and diabetic retinopathy?

13. Regarding the use of bevacizumab for diabetic retinopathy in Canada, which statement is correct?

14. A meta-analysis comparing RAAS inhibitors for diabetic retinopathy (21 RCTs, 13,823 participants) reached what conclusion regarding ACE inhibitors versus ARBs?

15. A patient is being considered for intravitreal steroid therapy for diabetic macular edema. Which adverse effects are associated with intraocular steroid treatment?

16. Which anti-VEGF agent demonstrated superiority in participants with worse baseline visual acuity in the head-to-head Protocol T study?

17. A normotensive patient with type 2 diabetes asks whether they should take an ACE inhibitor specifically to prevent retinopathy. Based on current evidence, what is the most appropriate response?

18. A 35-year-old woman with type 1 diabetes for 12 years and mild nonproliferative retinopathy is planning pregnancy. Her A1C is 8.2%. Based on understanding of risk factors, which statement best describes the retinopathy risk during pregnancy?

19. A 9-year-old child was diagnosed with type 1 diabetes at age 6. The parents ask about retinopathy screening. Based on the evidence, which statement is most accurate?

20. Which of the following is NOT a recognized risk factor for the development or progression of diabetic retinopathy?

21. A 45-year-old with type 1 diabetes for 18 years develops severe vitreous hemorrhage. According to the DRVS, what is the recommended approach?

22. What is the prevalence rate of proliferative retinopathy in people with type 1 diabetes?

23. A patient with type 1 diabetes and a history of poor glycemic control (A1C 10.5%) wants to achieve tight glucose control rapidly. What should you counsel regarding retinopathy?

24. According to landmark trials (DCCT and UKPDS), for how long do the beneficial effects of intensive glycemic control persist after completion of the trials?

25. What technology has encouraged the terminology “centre-involving” diabetic macular edema (DME)?

26. Diabetic retinopathy is the most common cause of incident blindness (legal) in which population?

27. A 42-year-old patient with type 2 diabetes has been on simvastatin for cardiovascular protection. They have established mild retinopathy. Based on the FIELD and ACCORD Eye studies, if fenofibrate is added, approximately how many patients would need to be treated to prevent one retinopathy progression event over 4 years?

28. A patient with type 2 diabetes has had two annual eye exams showing no retinopathy. What is the recommended rescreening interval?


 

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CDE Diabetes

Study Guide: Retinopathy (Chapter 30)

1. Overview & Epidemiology

Diabetic Retinopathy (DR) is the leading cause of new cases of blindness in adults aged 20–65 years in North America.

  • Risk Factors: The development and progression of DR are primarily driven by:

    • Duration of diabetes: The strongest predictor.

    • Glycemic control (A1C): Better control reduces risk.

    • Hypertension: Elevated BP accelerates progression.

    • Dyslipidemia: Associated with hard exudates and vision loss.

2. Pathophysiology & Classification

DR progresses through distinct stages, characterized by damage to the small blood vessels in the retina.

  • Non-Proliferative Diabetic Retinopathy (NPDR):

    • Early: Microaneurysms (outpouching of capillaries).

    • Moderate/Severe: Intraretinal hemorrhages, hard exudates (lipid deposits), cotton wool spots (nerve fiber infarction), and venous beading.

    • Key Feature: Absence of new blood vessels.

  • Proliferative Diabetic Retinopathy (PDR):

    • Key Feature: Neovascularization (growth of new, fragile blood vessels) on the retina or optic disc.

    • Risk: These vessels bleed easily (vitreous hemorrhage) and cause fibrosis, leading to tractional retinal detachment and severe vision loss.

  • Diabetic Macular Edema (DME):

    • Fluid leakage/swelling in the macula (the center of vision).

    • Can occur at ANY stage (NPDR or PDR) and is the most common cause of visual impairment in people with diabetes.

3. Screening Recommendations

Screening allows for early detection and treatment to prevent blindness. Visual acuity testing alone is insufficient; a comprehensive dilated eye exam is required.

A. Type 1 Diabetes

  • Start: 5 years after diagnosis (usually not before puberty).

  • Frequency: Annually.

B. Type 2 Diabetes

  • Start: At diagnosis.

  • Frequency: Every 1–2 years. (Interval can be extended to 2 years if there is no retinopathy and glycemic control is stable).

C. Pregnancy (Type 1 or Type 2)

  • Planning: Screen prior to conception.

  • During Pregnancy: Screen in the first trimester.

  • Follow-up: As determined by the eye specialist (DR can progress rapidly during pregnancy).

  • Note: This does not apply to Gestational Diabetes (GDM), as they are not at increased risk for DR during pregnancy.

4. Prevention & Management

Primary prevention focuses on systemic factors, while secondary treatment targets the eye directly.

Systemic Management (The “ABC”s):

  • A1C: Optimal glycemic control slows the onset and progression of retinopathy.

  • Blood Pressure: Control (<130/80 mmHg) is critical.

  • Cholesterol: Fenofibrate has been shown to slow progression of retinopathy (FIELD and ACCORD-Eye trials), particularly in those with mild-to-moderate NPDR, independent of lipid levels.

Ocular Treatment Options:

  1. Laser Photocoagulation:

    • Pan-Retinal Photocoagulation (PRP): Used for PDR. Burns the peripheral retina to stop neovascularization.

    • Focal/Grid Laser: Used for DME (historically the standard, now often second-line).

  2. Intraocular Pharmacotherapy (Injections):

    • Anti-VEGF Agents (e.g., ranibizumab, aflibercept, bevacizumab): Now first-line therapy for center-involving DME with vision loss. They reduce fluid and improve vision.

    • Steroids: For resistant cases.

  3. Vitrectomy: Surgery to remove blood (vitreous hemorrhage) or scar tissue (retinal detachment).

5. Diabetes Canada 2018 Clinical Practice Guidelines Recommendations

Key takeaways from the “Recommendations” section (Page S215).

  1. Screening Intervals:

    • Type 1: Start 5 years after diagnosis, then annually [Grade A, Level 1].

    • Type 2: Start at diagnosis, then every 1–2 years [Grade A, Level 1].

  2. Screening Method: Assessments should be performed by an experienced professional (optometrist/ophthalmologist) through dilated pupils [Grade D, Consensus].

  3. Pregnancy: Screen women with T1D or T2D pre-conception, in the first trimester, and as needed thereafter [Grade D, Consensus].

  4. DME Treatment: Intraocular anti-VEGF therapy is recommended as first-line for center-involving diabetic macular edema with vision loss [Grade A, Level 1].

  5. Fenofibrate: Fenofibrate (in addition to statins) may be used in patients with Type 2 diabetes to slow the progression of established retinopathy [Grade A, Level 1].

Reference:

Altomare F, Kherani A, Lovshin J. Retinopathy. Canadian Journal of Diabetes. 2018;42:S210-S216. doi:10.1016/j.jcjd.2017.10.027
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CDE Diabetes

Flashcards: Chronic Kidney Disease in Diabetes (Chapter 29 – 2025 Update)

The 2025 Guidelines Update marks a fundamental shift in practice—moving away from a glucocentric view toward a comprehensive strategy focused on delaying renal progression and reducing cardiovascular risk. These flashcards are designed to help pharmacists and healthcare professionals quickly recall the updated diagnostic criteria, the new foundational role of SGLT2 inhibitors, and the specific indications for non-steroidal mineralocorticoid receptor antagonists (MRAs).

Key Topics Covered:

  • Diagnostic Criteria: Memorizing the thresholds for CKD diagnosis: an eGFR <60 mL/min/1.73 m² and/or a random Urine Albumin-to-Creatinine Ratio (UACR) 2.0 mg/mmol on repeated measures.

  • Foundational Therapy: Understanding the recommendation to use SGLT2 inhibitors as a primary treatment for renoprotection in eligible patients, regardless of glycemic control.

  • New Agents: Identifying finerenone (a non-steroidal MRA) as an add-on therapy for patients with Type 2 diabetes and CKD who remain at risk despite standard care.

  • RAAS Blockade: Recalling the rule to use an ACE inhibitor or an ARB for albuminuric patients, but never to combine them due to hyperkalemia and acute kidney injury risk.

  • Sick Day Management: Reviewing the “SADMANS” protocol for holding medications during acute illness to prevent acute kidney injury.

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CDE Diabetes

Practice Exam: Chronic Kidney Disease in Diabetes (Chapter 29 – 2025 Update)

Diabetes remains the leading cause of kidney failure in Canada. The 2025 Guidelines Update represents a significant evolution in care, moving beyond simple glucose control to a “kidney-protective” strategy that utilizes newer pharmacotherapies to delay progression and reduce cardiovascular risk.

This practice exam tests your ability to apply the latest screening protocols, diagnostic criteria, and the expanded treatment algorithms for patients with varying stages of renal impairment.

Key Concepts Covered in This Exam:

  • Screening & Diagnosis: Mastering the criteria for diagnosing Chronic Kidney Disease (CKD) using the Urine Albumin-to-Creatinine Ratio (UACR) and eGFR, and distinguishing persistent albuminuria from transient causes.

  • Renoprotective Pharmacotherapy: Applying the updated recommendations for SGLT2 inhibitors as a foundational treatment for delaying CKD progression, even in patients without optimal glycemic control.

  • Non-Steroidal MRAs: Identifying the specific indications for finerenone (a non-steroidal mineralocorticoid receptor antagonist) in patients with Type 2 diabetes and CKD who remain at risk despite standard-of-care treatment.

  • RAAS Blockade: Reviewing the use of ACE inhibitors or ARBs for albuminuric patients and the critical caution against using them in combination.

  • “Sick Day” Management: Recognizing when to temporarily pause medications (like SADMANS) to prevent acute kidney injury during intercurrent illness.

Please go to Practice Exam: Chronic Kidney Disease in Diabetes (Chapter 29 – 2025 Update) to view this quiz

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Study Guide: Chronic Kidney Disease in Diabetes (2025 Update – Chapter 29)

1. Overview & Diagnosis

Chronic Kidney Disease (CKD) is a frequent complication of diabetes, affecting ~50% of people with Type 2 diabetes and 30% of those with Type 1 diabetes. It is a major driver of cardiovascular (CV) mortality.

  • Definition of CKD:

    • eGFR:

    • AND/OR

    • Albuminuria: Urine Albumin-to-Creatinine Ratio (ACR)

    • Duration: Abnormalities must persist for > 3 months.

  • Screening Frequency:

    • Type 1 Diabetes: Start screening 5 years after diagnosis, then annually.

    • Type 2 Diabetes: Start screening at diagnosis, then annually.

    • Method: Random urine ACR + Serum Creatinine (to calculate eGFR).

  • Diagnosis Confirmation:

    • A single abnormal ACR is not sufficient. It must be confirmed with 2 out of 3 tests being abnormal over a 3-month period.

    • False Positives: Exercise, infection, fever, congestive heart failure, menstruation, and acute hyperglycemia can transiently elevate ACR.

2. Comprehensive Management (The "Pillars")

The 2025 guidelines emphasize a multi-pillar approach to delay progression and reduce CV risk.

A. Glycemic & Blood Pressure Control

  • A1C Target: Individualized (usually ).

  • Blood Pressure: Target .

B. Pharmacotherapy: The 4 Classes

  1. ACE Inhibitors (ACEi) or ARBs (RAAS Blockade):

    • Indication: Recommended for people with diabetes, hypertension, and albuminuria (ACR ).

    • Caution: Monitor creatinine and potassium. A rise in creatinine of up to 30% is acceptable upon initiation; do not stop unless it exceeds this. Do not combine ACEi and ARB.

  2. SGLT2 Inhibitors (Flozins):

    • Indication: Strongly recommended for adults with Type 2 Diabetes and CKD (eGFR ) to reduce CKD progression and heart failure.

    • Effect: Reduces intraglomerular pressure.

    • Initiation: Can be started if eGFR and continued until dialysis is required.

  3. Mineralocorticoid Receptor Antagonists (MRA) – Finerenone:

    • Indication: For adults with Type 2 Diabetes and CKD (eGFR ) who have persistent albuminuria despite maximizing ACEi/ARB and SGLT2i.

    • Type: Finerenone is a non-steroidal MRA (unlike spironolactone) and has less risk of side effects but still requires potassium monitoring.

  4. GLP-1 Receptor Agonists:

    • Role: Recommended for CV risk reduction in T2D and CKD. Can be used if SGLT2i is contraindicated or not tolerated.

    • Note: Dose adjustment may be needed for renal function depending on the specific agent.

3. Acute Kidney Injury (AKI) & Sick Days

Educating patients on preventing AKI during intercurrent illness is a core CDE competency.

  • SADMANS Rule: Patients should temporarily stop the following medications when sick (vomiting, diarrhea, unable to hydrate):

    • S = Sulfonylureas

    • A = ACE Inhibitors

    • D = Diuretics / Direct Renin Inhibitors

    • M = Metformin

    • A = ARBs

    • N = NSAIDs

    • S = SGLT2 Inhibitors

4. Management of Hyperkalemia

Hyperkalemia is a barrier to using life-saving drugs (RAAS inhibitors, MRAs).

  • Diet: First-line management is dietary restriction of potassium.

  • Binders: If hyperkalemia persists, consider Potassium Binders (Patiromer or Sodium Zirconium Cyclosilicate) to allow continuation of RAAS blockade rather than stopping the medication.

5. Referral to Nephrology

Referral is indicated if:

  • Progressive Loss: Rapid decline in eGFR ().

  • Advanced Disease: eGFR .

  • Uncertainty: Etiology of kidney disease is unknown.

  • Management Issues: Unable to control BP or hyperkalemia.

6. 2025 Diabetes Canada Clinical Practice Guidelines Recommendations

Key takeaways from the “Recommendations” section.

  1. Screening: Screen annually with random urine ACR and eGFR [Grade D, Consensus].

  2. SGLT2 Inhibitors: Recommended for patients with T2D and CKD (eGFR ) to reduce progression of kidney disease and CV events [Grade A, Level 1A].

  3. Finerenone: Recommended for patients with T2D and CKD (ACR > 3.0 mg/mmol) with normal potassium, to reduce progression of CKD and CV events [Grade A, Level 1A].

  4. RAAS Blockade: ACEi or ARB should be used in patients with diabetes, hypertension, and clinical albuminuria [Grade A, Level 1].

  5. Hyperkalemia: In patients with hyperkalemia limiting the use of RAAS inhibitors/MRAs, use potassium binders (Patiromer or SZC) to enable continuation of therapy [Grade B, Level 2].

Reference:

Tobe SW, Bajaj HS, Tangri N, et al. Chronic Kidney Disease in Diabetes: A Clinical Practice Guideline. Canadian Journal of Diabetes. 2025;49(2):73-86.e14. doi:10.1016/j.jcjd.2025.01.004
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CDE Diabetes

Flashcards: Treatment of Diabetes in People with Heart Failure (Chapter 28)

Heart failure is a frequent and often fatal complication of diabetes. The 2018 Clinical Practice Guidelines mark a major shift in treatment, prioritizing agents that specifically reduce heart failure hospitalizations and identifying those that may cause harm. These flashcards are designed to help pharmacists and healthcare professionals memorize the safety profiles and outcome data for SGLT2 inhibitors, TZDs, and DPP-4 inhibitors in this high-risk population.

Key Topics Covered:

  • Therapeutic Benefit: Identifying the specific role of SGLT2 inhibitors (empagliflozin, canagliflozin, dapagliflozin) in reducing the risk of heart failure hospitalization in patients with established cardiovascular disease.

  • Agents to Avoid: Recognizing the risk of fluid retention and heart failure exacerbation associated with Thiazolidinediones (TZDs).

  • Safety Signals: Recalling the specific concern regarding saxagliptin and increased heart failure hospitalization rates seen in the SAVOR-TIMI 53 trial.

  • Epidemiology: Understanding that diabetes is an independent risk factor for heart failure (“diabetic cardiomyopathy”) and significantly worsens prognosis.

  • Neutral Agents: Knowing which drug classes (e.g., most GLP-1 receptor agonists) are considered safe/neutral regarding heart failure outcomes .

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CDE Diabetes

Practice Exam: Treatment of Diabetes in People with Heart Failure (Chapter 28)

Heart failure is one of the most common and serious cardiovascular complications of diabetes, with up to 40% of people with heart failure having comorbid diabetes. The 2018 Clinical Practice Guidelines mark a significant paradigm shift, prioritizing the use of specific glucose-lowering agents that have been proven to reduce heart failure hospitalizations, while identifying others that may cause harm.

This practice exam tests your ability to navigate these critical therapeutic choices, ensuring you can select the safest and most effective regimens for this vulnerable patient population.

Key Concepts Covered in This Exam:

  • The SGLT2 Inhibitor Benefit: Understanding the recommendation to use SGLT2 inhibitors (empagliflozin, canagliflozin, dapagliflozin) in patients with clinical cardiovascular disease to specifically reduce the risk of heart failure hospitalization.

  • Agents to Avoid: Identifying Thiazolidinediones (TZDs) as agents that cause fluid retention and are associated with an increased risk of heart failure.

  • DPP-4 Inhibitor Caution: Recognizing the specific safety signal associated with saxagliptin, which was shown to increase the rate of hospitalization for heart failure in the SAVOR-TIMI 53 trial.

  • Epidemiology and Risk: Acknowledging that heart failure is a major driver of mortality in diabetes and that the presence of diabetes significantly worsens the prognosis for patients with established heart failure.

  • Neutral Agents: Knowing which other antihyperglycemic agents (such as most GLP-1 receptor agonists) have demonstrated safety—but not necessarily benefit—regarding heart failure outcomes.

Please go to Practice Exam: Treatment of Diabetes in People with Heart Failure (Chapter 28) to view this quiz

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CDE Diabetes

Study Guide: Treatment of Diabetes in People with Heart Failure (Chapter 28)

1. Overview & Pathophysiology

Heart failure (HF) is a frequent and serious comorbidity in diabetes.

  • Incidence: The incidence of heart failure is 2- to 4-fold higher in people with diabetes compared to those without.
  • Diabetic Cardiomyopathy: Diabetes can cause heart failure independently of coronary artery disease or hypertension. This is known as “diabetic cardiomyopathy”.
  • Types: Heart failure can occur with Reduced Ejection Fraction (HFrEF, LVEF <40%) or Preserved Ejection Fraction (HFpEF, LVEF >50%).

2. Diagnosis

Diagnosis relies on typical signs/symptoms (edema, shortness of breath) combined with objective evidence (Echo, Chest X-ray).

  • Biomarkers: Brain Natriuretic Peptide (BNP) or NT-pro-BNP are useful to aid diagnosis when clinical uncertainty exists.
  • Screening: Current evidence is mixed, and there is no clear consensus to routinely screen asymptomatic people with diabetes for HF using BNP testing.

3. Antihyperglycemic Agents & Heart Failure (High Yield)

The choice of diabetes medication is critical in this population. You must know which drugs help, which are neutral, and which can harm.

A. The “Good” (Benefit demonstrated)

  • SGLT2 Inhibitors:
    • Empagliflozin: Demonstrated a 35% reduction in heart failure hospitalization in the EMPA-REG OUTCOME trial.
    • Canagliflozin: Reduced heart failure hospitalization in the CANVAS trial.
    • Mechanism: Benefits appear independent of glucose lowering.
    • NOTE: This guideline chapter was published prior to the EMPEROR-REDUCED (Empagliflozin) and DAPA-HF (Dapagliflozin) trials were published

B. The “Neutral” (Generally Safe)

  • Metformin:
    • Safe and effective. Studies show people with HF fare as well or better on Metformin than other agents.
    • Caveat: Use with caution in renal dysfunction (eGFR > 30 mL/min is generally safe) and stop if acute illness/dehydration occurs.
  • GLP-1 Receptor Agonists:
    • Liraglutide (LEADER), Lixisenatide (ELIXA), and Semaglutide (SUSTAIN-6) showed neutrality for heart failure hospitalization.
    • Note: Liraglutide showed no benefit in patients with established HFrEF (FIGHT study).

C. The “Bad” / Caution Required (Potential Harm)

  • Thiazolidinediones (TZDs):
    • Rosiglitazone & Pioglitazone: Cause fluid retention. Rosiglitazone doubled the risk of HF death/hospitalization in the RECORD trial.
    • Contraindication: Avoid in people with NYHA Class I–IV heart failure.
  • DPP-4 Inhibitors (Saxagliptin):
    • Saxagliptin: The SAVOR-TIMI 53 trial showed an increased risk of hospitalization for heart failure.
    • Warning: Health Canada and FDA issued warnings to consider discontinuing Saxagliptin if HF develops.
    • Other DPP-4s: Sitagliptin (TECOS) and Alogliptin (EXAMINE) were neutral.

4. Heart Failure Medications in Diabetes

People with diabetes should receive the same standard HF therapies as those without diabetes.

  • Beta-Blockers: Carvedilol, Bisoprolol, and Metoprolol Succinate reduce mortality.
    • CDE Pearl: Carvedilol may improve glycemic control compared to other beta-blockers.
  • RAAS Blockade (ACEi/ARB/ARNI): Effective but requires monitoring.
    • Risk: People with diabetes are at higher risk for hyperkalemia and worsening renal function.
    • Management: Halve the starting dose and monitor electrolytes/creatinine within 7–10 days of initiation.

5. 2018 Diabetes Canada Clinical Practice Guidelines Recommendations

Key takeaways from the “Recommendations” section (Page S200).

  1. Standard of Care: Individuals with diabetes and heart failure should receive the same heart failure therapies (ACEi, Beta-blockers, etc.) as those without diabetes [Grade D, Consensus].

  2. Metformin: May be used in people with T2D and heart failure (unless contraindicated/renal failure) [Grade C, Level 3]. Stop if renal function significantly worsens [Grade D].

  3. Avoid TZDs: For people with NYHA class I–IV, exposure to TZDs should be avoided [Grade A, Level 1].

  4. SGLT2 Inhibitors: In adults with T2D and clinical CVD (and eGFR > 30), an SGLT2 inhibitor with demonstrated benefit may be added to reduce the risk of heart failure hospitalization.

  5. Dosing Caution: In adults with diabetes and HF with eGFR < 60 mL/min, starting doses of ACEi or ARBs should be halved [Grade D, Consensus].

Reference:

Connelly KA, Gilbert RE, Liu P. Treatment of Diabetes in People With Heart Failure. Canadian Journal of Diabetes. 2018;42:S196-S200. doi:10.1016/j.jcjd.2017.10.026