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Practical Diabetes Pearls

One of the hardest barriers to treat diabetes is the fear of starting insulin on patients. Not only do you have patient barriers but you may also have provider barriers. Her will discuss mainly patient barriers to starting insulin.

Addressing insulin fears

Patients come into the visit with many pre-conceived ideas about medications but especially insulin. The first step is to try to find out why they don’t want insulin, is it fear of needles or is it fear of insulin itself?

Is it fear of needles or fear of insulin?

Determining the root cause of patients’ fears or ambivalence toward insulin therapy can allow for more specific discussion, intervention and resolution.

Fear of needles:

Fear of pain or discomfort
  • Compare the sensation to the current experience.
  • Perform a mock injection with saline and an insulin syringe, and share your personal experience (if any) with subcutaneous injections. If appropriate, go through the exercise with the patient in the office with saline
Fear of exposures
  • Review low risk for infection, explain the sterility of products and educate on safe injection techniques

Fear of insulin:

• Associating need for insulin with personal failure

Have frequent discussions and provide reassurances that the progression of diabetes and need for insulin is normal, and not a reflection of personal failure.

• Worry about side effects, costs, interference with life/routine, whether insulin will work or “fail”, and others

Early conversations can elucidate concerns, and allows time for patient-centered discussions and interventions to address worries and fears.

Include family members and other team members to address specific needs.

• Former experience with a friend or loved-one, e.g. “My uncle started insulin and then he needed to have his leg amputated.”

Review importance of balancing personalized goals of therapy with quality of life and show commitment to shared-decision making.

As part of early education, patients should be introduced to the possibility of insulin for treatment. Weather is because their disease state has progressed or they are sick and in the hospital or they have symptoms suggestive of insulin deficiency (weight loss, polyuria/polydipsia)

Fear of Hypoglycemia

Many times they feel anxious and feel like they may even die. When patients develop this fear, they will often skip their insulin doses or even reduce doses to avoid low blood sugars. In the same way they may not want to restart insulin if they had a bad hypoglycemic episode.

Many patients once they have experienced hypoglycemia will become very afraid of the feeling they get during low blood sugars.

Reassure patients that this time you will start the dosing low and go slow, review what to do if they get a low blood sugars

Talking Points For When You Start Insulin

  • When insulin is indicated, explain why and how it will be helpful. Reinforce that the need for insulin does not represent a personal failure.
  • Keep the conversation(s) dynamic and patient-centered. Use open-ended questions and reflective listening to learn the patient’s expectations, impressions, and fears about insulin. Tailor the conversation to their needs.
  • Share your opinion as their provider, and show that you find value in the patient’s perspective.
  • Involve the patient’s caregivers and all members of the patient’s care team in the conversation(s) (nurses, medical assistance, support staff, etc).

“Many patients have told me that once they get the hang of it, injecting the insulin is actually easier and less painful than checking your blood sugar with the fingerstick. I even tried it myself!”

Many times Provider barriers can also become a problem. Providers can delay starting insulin for fear of complications like severe hypoglycemia, lack of time for teaching or close follow-up, unsure how to start or adjust insulin, and complexity of newer insulins. This is where Pharmacists can have a role to help educate not only the patients but also the providers. Pharmacists can also help adjust insulin doses and monitor patients closely to avoid complications or side effects.

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What is Atrial Fibrillation

January C.T, et al. J. Am Coll Cardio. 2014:21

What is Atrial Fibrillation?

  • Supraventricular arrhythmia:
    • Supraventricular—originate above bundle of His, char by abnormal P waves w/ normal QRS and QTc intervals
  • Uncoordinated atrial activation and ineffective atrial contraction
  • Irregularly, irregular pulse

Atrial Fibrillation (or A. Fib)

  • Most common cardiac arrhythmia
  • EKG: irregular R-R intervals, no distinct repeating p waves, and irregular atrial activity
  • Worldwide: 33.5 million, ~3-6 million in US
  • Prevalence increases with age (>65), 3% of men and 2% of women
  • Contributes to >99,000 deaths per year
  • 20% of patients who have a stroke associated with AF receive an AF diagnosis at the time of stroke or shortly thereafter

Annual Death Rates from AF (2015)

•AF was the underlying cause of death in ~24,000 people and listed on ~150,000 US death certificates

•In adjusted analyses from the Framingham Heart Study, AF was associated with an increased risk of death in both males (OR, 1.5; 95% CI, 1.2-1.8) and females (OR, 1.9; 95% CI, 1.5-2.2)

–AF diminishes the survival advantage typically observed in females

Classification

  • Paroxysmal (occasional)
    • Terminates spontaneously or with intervention within 7 days
  • Persistent
    • Continuous—sustained > 7 days
  • Longstanding persistent
    • Continuous— > 12 months in duration
  • Permanent
    • Acceptance of AF: Permanent: when patient and doctor make joint decision to stop further attempts to restore and/or maintain sinus rhythm
    • Represents a therapeutic attitude vs. an inherent pathophysiologic attribute of AF
  • Attitudes and acceptance of AF may change as symptoms, efficacy of therapies, and patient/clinician preferences evolve

Nonvalvular

  • In absence of rheumatic mitral stenosis, mechanical/bioprosthetic heart valve, or mitral valve repair
  • Important because it guides therapy

January CT, et al. J Am Coll Cardiol. 2014;64:21

Strokes in AF Lead to More Disability

Lin HJ, et al. Stroke 1996;27(10):1760-1764. Tu HT, et al. Cerebrovasc Dis. 2010;30(4):389-395.

  • Larger infarcts (52 vs. 15 ml, P=0.05)
  • Higher mortality (HR= 1.84)
  • More severe hemorrhagic transformation (29% vs. 5%, P=0.002)

Risk Factors and Underlying Comorbidities to Address in Chronic AF Management

Major risk factors

  • Older age
  • Obesity
  • (Borderline) hypertension

Other risk factors

•(Pre) diabetes

•Heart failure

•Prior cardiothoracic surgery

•Smoking

•Prior stroke

•Obstructive sleep apnea

•Drug use Alcohol consumption

•Vascular disease

•Hyperthyroidism

•Lipid profile

•Coronary artery disease

•Physical inactivity

•Chronic kidney disease

•COPD

•Valve disease

•Inflammatory diseases

Brandes A, et al. Arrhythm Electrophysiol Rev.2018;7(2):118-127.Steinhubl S, et al. JAMA. 2018;320(2):146-155.

Pathophysiology

AF occurs when structural and/or electrophysiological abnormalities alter atrial tissue to promote abnormal impulse formation and/or propagation.

Heart has Purkinje fibers (specialized cardiac muscle fibers that rapidly transmit impulses from the atrioventricular node to the ventricles)

  • Fibers are split into 2 branches

Normal

  • Electrical impulse (action potential) travels down both branches
  • Meet in the connecting p/w and cancel each other out

Reentry

  • When there is a block in one of the branches, the AP only travels down one branch leads to No longer canceled out
  • Travels retrograde through the block and can then travel down the 1st branch again
  • leads to indefinite propagation leads to abnormal impulses in AF

These abnormalities are caused by diverse pathophysiological mechanisms

A.Fib Normal vs re-entry

AF begets AF

Atrial structural abnormal

  • Any disturbance in atrial structure that increases susceptibility to AF
  • Most commonly d/t extracardiac factors that increases left atrium pressure, cause atrial dilation and alter wall stress
  • Structural abnormal à alter impulse conduction/refractoriness

Mechanisms of AF

Mechanism of A. Fib

Electrophysiological mech

  • Triggers of AF
    • Abnormal focal discharges initiate AF
    • Rapidly firing foci most commonly from left atrium
    • Conduction abnormal that promote reentry d/t depolarized resting potentials that promote sodium channel inactivation
    • Abnormal intracellular calcium handling d/t diastolic calcium leak from sarcoplasmic reticulum, which can trigger delayed after-depolarization
  • ANS
    • Activation of para and/or sympathetic NS can provoke atrial arrhythmias
    • Sympathetic: activates beta-1 adrenergic R
      • Cardiac excitatory effects: increased conduction, contraction, irritability of foci
    • Parasympathetic: activates cholinergic R
      • Cardiac inhibitory effects:

Pathophysiological mechanisms

  • Atrial tachycardia remodeling: AF begets AF
  • Inflammation and ox stress
    • Inflammationà increased concentration of C-reactive protein (marker of inflammation, high-sensitivity C-rp assay can determine risk for CAD)
  • RAAS
    • Angiotensin II, ACE and aldosterone are synthesized locally in atrial myocardium and are increased during AF

Automaticity: ability of cardiac muscle to spontaneously depolarize in a reg constant manner

Key Points

•AF is common

•Prevalence increases with age

•Proper diagnosis and classification are key to properly manage arrhythmia and minimize stroke risk

Symptoms

  • Fluttering in the chest
  • Feeling faint, weakness, syncope

A.Fib increases your risk of thromboembolic stroke

Treatment

  • Rate Control
    • Control ventricular rate with beta blockers or non-DHP calcium channel blockers and AV nodal ablation
      • Medications
      • Arteriovenous (AV) junction ablation + pacemaker (PPM)
  • No attempt made to restore SR
  • Rhythm Control
    • Long-term management with cardioversion, antiarrhythmics, and radiofrequency catheter ablation
    • Attempt made to restore SR
  • Anticoagulation
    • Prevention of thromboembolism

BB: block sympathetic tone (atenolol, metoprolol, nadolol, propranolol, carvedilol)

CCB: direct AV nodal effects, block L-type Ca channels (diltiazem, verapamil)

January CT, et al. J Am Coll Cardiol. 2014;64:21

What Is AF Ablation?

•Cardiac ablation: Procedure using energy to create lesions (resulting in scarring) in the atria with the goal of stopping abnormal electrical conduction

•Pulmonary vein (PV) isolation: Electrical isolation of the PVs, which are well-known triggers for AF and are the key lesion set for an AF ablation

•Cavo-tricuspid isthmus ablation: Done in patients with concomitant atrial flutter

•Types of ablation:

–Catheter-based: Minimally invasive

–Surgical: Maze, minimally invasive, usually concomitant with open-heart surgeries (e.g., CABG)

–Hybrid approach: Catheter-based + minimally invasive surgery

Calkins H, et al. Heart Rhythm. 2017;14(10);e275-e444.

AADs

•Recurrence rates

–Amiodarone: 35%

–Sotalol: 63%

–Propafenone: 63%

•Adverse events

–Amiodarone: 18%

–Sotalol/propafenone: 11%

 Singh BN, et al. N Engl J Med. 2005;352:1861-1872.Pedersen OD, et al. Circulation. 2001;104:292-296.Freemantle N, et al. Europace. 2011;13:329-345.Piccini JP, et al. J Am Coll Cardiol. 2009;54:1089-1095.The AFFIRM First Antiarrhythmic Drug Substudy Investigators.J Am Coll Cardiol. 2003;42:20-29.Lafuente-Lafuente C, et al.Cochrane Database Syst Rev. 2007;(4):CD005049.

Key Points

•Rate control is an option for patients with few symptoms and in whom maintaining SR will be risky, challenging, or unsuccessful

–Can be achieved with medications or AV junction ablation and pacing

•Rhythm control is an option for symptomatic patients, or those who develop a cardiomyopathy–Better option for younger patients with less advanced heart disease

–Can be achieved with AADs or catheter ablation

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Exercise Recommendations for Patients with Diabetes

Why is Exercise Important in Patients with Diabetes?

Exercise is a very important part of getting blood sugars under control and one that is often overlooked, put aside or not done at all.

The American Diabetes Association exercise recommendations are:

  • For most adults with type 1 and type 2 diabetes: 150 or more minutes per week of moderate-to-vigorous activity over at least 3 days per week with no more than 2 consecutive days without exercise.
  • Shorter durations (minimum 75 min/week) of vigorous-intensity or interval training may be sufficient for younger and more physically fit individuals.
  • Adults with type 1 and type 2 diabetes should perform resistance training in 2-3 sessions/week on nonconsecutive days.

What if You Don’t Exercise but Want to Start?

For those who do not exercise at all but want to start, it is important to start slowly and safe. It is always a good idea to check with your doctor before starting any exercise routine.

It is important to start by being more active, slowly adding exercise like walking. The key is to be less sedentary and start moving more.

Start by Moving More

Research found that sitting too much for long periods of time is harmful to our health especially related to heart health, mental health and increased risk for becoming disabled.

Just getting up once every 30 minutes to stretch or walk around the house or workplace is better than sitting for hours. Take every opportunity you can to get up and move.

If you don’t exercise at all, getting motivated is half the battle. Once you start being more active, you’ll find that it isn’t as hard to keep going — you’ll feel better and have more energy.

Aerobic exercise, strength training, flexibility exercises/stretching, balance exercises, and activity throughout the day are the types of activities recommend for people with diabetes.

Exercise should be part of your Diabetes Action Plan and you can make it one of your Health goals.

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Celebrate Women Pharmacists

March is Women’s History Month. As a Pharmacist, I want to mark this month by recognizing and honoring the many women that have contributed to the success and advancement of the pharmacy profession.

I want to start by giving a great thanks to Dr. Suzanne Rabi Soliman, PharmD. Who worked very hard to make October 12 National Women Pharmacist Day, October is American Pharmacist Month, and she chose the number 12 in honor of Elizabeth Greenleaf. Ms. Greenleaf was the first woman pharmacist in America and had 12 children. As a Pharmacist and mom, Dr. Soliman found Mrs. Greenleaf to be inspiring and therefore chose October 12 as the day to honor Women Pharmacist.

Recently Dr. Soliman wrote an article about being a Pharmacist and a Mom which you can read by clicking the following link: http://www.pharmacytimes.com/news/are-you-a-pharmacist-and-a-mom.
Jean Kennedy Irvine, was born in 1877 in Hawick. Her first post was an assistant pharmacist to the Glasgow Apothecaries Company to which she subsequently became Chief Pharmacist. She was the first woman president of the staff side of Whitley Council for National Insurance administrative, technical and clerical services. She was the first woman elected to the presidency of the insurance Committee Officers Association for England and Wales.

Another pioneer is the first female pharmacist in the United States. After graduating from the Woman’s Medical College of Philadelphia in 1857, Susan Hayhurst served on the College’s staff and ran its pharmaceutical department for many years. In 1883, at the age of 63, Susan Hayhurst became the first woman to graduate from the Philadelphia College of Pharmacy.

Ella Stewart (born in Stringtown, West Virginia). Stewart wished to attend the University of Pittsburgh’s School of Pharmacy but was met with discrimination when she was told admissions were closed. She persisted, however, and although segregated from other students, she graduated with high marks passing her state exam in 1916, to become the first licensed African-American female pharmacist in Pennsylvania and one of the earliest practicing African-American female pharmacists in the country.

Elizabeth Marshall was born in 1786, the second USA woman to be Pharmacist. In 1805 she took over the drugstore owned by her grandfather and restore the struggling business to a successful business.
Mary Munson Runge born in 1928, graduated from Xavier University of Louisiana in 1948. She practiced pharmacy for 21 years, she was the first woman and African American to serve as president of the American Pharmacist Association (APhA) in 1979.

This is only a small group of the many women who have been part of pharmacy through the years. Mary Euler, PharmD, FAPhA, Professor and Associate Dean for Student Services at the West Virginia University School of Pharmacy noted that in the early 1900s, many pharmacy programs opened with all men; a woman in the program would have been a rarity. During World War II, a temporary increase of women in the profession occurred as men were not as available. In the 30 years that Dr. Euler has been in pharmacy academia, she has seen a gradual shift from 60% men/40% women to now about 40% men/60% women.

The success of women pharmacists today can in many ways be credited to the women in our past. These women were instrumental in not only increasing female pharmacist representation but also advancing the profession.