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PHAR 152* > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Are outcomes for diabetes improving?

A

Yes, they have never been better

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2
Q

What is the official definition of diabetes mellitus?

A

A metabolic disorder characterized by the presence of hyperglycemia due to defective insulin secretion, insulin action, or both

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3
Q

What is the prevalence of Diabetes?

A

4 million diagnosed (10% of population), but about 30% have diagnosed, undiagnosed, or prediabetes

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4
Q

How has the prevalence of diabetes among adults in Canada shifted over the last 50 years?

A

It has almost doubled from 14% in 1970 to 29% in 2021

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5
Q

What are some of the reasons for the shift in the number of Canadian adults with diabetes?

A

Demographic changes (Canadians are getting older, and more people from risk populations are becoming Canadians)

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6
Q

What are the costs associated with diabetes?

A

Estimated economic impact: $30 billion/yr

Medical costs are 2-3x higher in those with diabetes

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7
Q

What are some complications associated with diabetes?

A

CVD (the main cause of death), kidney dysfunction, blindness, neuropathy, amputation)

80% will die from heart disease and stroke

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8
Q

How much can diabetes reduce life expectancy?

A

an estimated 5-15 years

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9
Q

What is the role of the pancreas in blood sugar maintenance?

A

Euglycemia (ideal blood sugar) is maintained by the following three hormones

Alpha (produce glucagon, account for 30% of islet cells)

Beta (produce insulin, account for 60% of islet cells)

Delta (produce somatostatin, account for 10% of islet cells)

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10
Q

View slides 13-14 to review the interplay of insulin and glucagon

A
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11
Q

What is the effect of insulin on skeletal muscle?

A

Muscle is the major site of glucose uptake, and insulin stimulates glucose uptake

Glucose is stored as glycogen in muscle and it is used in energy metabolism (glycogenesis)

Insulin also stimulates the production of proteins from amino acids.

Between meals, energy stored in proteins is harvested by breaking them down back into amino acids. These amino acids can undergo gluconeogenesis, producing glucose

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12
Q

What happens in diabetes with respect to skeletal muscle?

A

Glucose is never able to be taken up by skeletal muscle cells, therefore limiting energy sources

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13
Q

What is the effect of insulin on the liver?

A

The liver produces glycogen (product of insulin-induced uptake of glucose), and insulin release following a meal will stimulate the liver to pull glucose from the blood and form glycogen

Insulin also suppresses gluconeogenesis

If the amount of glucose entering the liver is more than the storage capacity for glycogen, insulin promotes its conversion to fatty acids

Between meals, glucagon is released. This hormone promotes glycogenesis and gluconeogenesis, producing glucose

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14
Q

What is the effect of insulin on adipose tissue?

A

Insulin is effectively a fat storing hormone

Excess carbs are converted into fatty acids and stored as triglycerides in adipose tissue

In starvation or insulin deficiency, fats break down and form ketones. These ketones can be used as an energy source (lipolysis)

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15
Q

What is the effect of insulin on the brain?

A

The brain gets all of its energy from glucose, but does not depend on insulin for glucose uptake.

The brain is not directly effected by insulin, but low blood sugar due to insulin activity can cause states of confusion to unconsciousness

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16
Q

What are the different classifications of diabetes covered in this course?

A

Prediabetes:
Impaired glucose tolerance (IGT)
Impaired fasting glucose (IFG)

Diabetes:
Type 1
Type 2

Gestational Diabetes

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17
Q

Describe Type 1 Diabetes Mellitus (T1DM)

A

Characterized by an absolute lack of insulin secretion

Primarily due to autoimmune beta-cell destruction

Typically, markers of immune destruction are present: islet cell antibodies and insulin antibodies.

Not uncommon to see patients with T1DM to also have other autoimmune diseases

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18
Q

Is Type 1 Diabetes (T1DM) a disease often seen in children?

A

Yes, it is most commonly has its incidence in patients under 25 (13-14 yo. peak)

But we can occasionally see cases that emerge in the sixth and seventh decade of life

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19
Q

In children with diabetes, most of them have Type 2 diabetes. True or False?

A

False, most children (95%) have Type 1 diabetes

Adults with diabetes on the other hand show Type 2 diabetes (90%) of the time

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20
Q

Are Type 1 Diabetes (T1DM) incidence rates falling now?

A

No, it appears that they have a doubling time of a few decades

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21
Q

What initiates Type 1 diabetes and the subsequent breakdown of beta cells?

A

This immunologic trigger remains elusive, perhaps due to exposure to a virus or toxin

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22
Q

Review slide 24 to closely see how Type 1 diabetes (T1DM) progresses in terms of beta cell function

A
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23
Q

When do symptoms in Type 1 Diabetes manifest?

A

After 80-90% of beta cells have been destroyed

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24
Q

What is the “honeymoon phase” in Type 1 Diabetes (T1DM)?

A

Following initial correction of hyperglycemia with exogenous insulin, causes endogenous insulin production to recover temporarily

This usually occurs in the days to weeks following starting insulin

This “recovery” is temporary, so insulin therapy and monitoring continues

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25
Q

What is significant about treatment in prediabetes?

A

Many trials have shown diabetes can be prevented in those with prediabetes via lifestyle modifications or medications. Many patients will revert to normoglycemia

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26
Q

What are the details of prediabetes diagnosis in terms of relevant lab values?

A

Fasting plasma glucose (mmol/L): 6.1-6.9, IFG (impaired fasting glucose)

Glucose levels 2h after 75g of glucose is consumed (mmol/L): 7.8-11.0, IGT (impaired glucose tolerance)

A1C%: 6.0-6.4, Prediabetes

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27
Q

What is the relevance of A1C% and risk for developing diabetes?

A

Slight increased in A1C% = Significant changes in risk for diabetes

ex. A1C% (5.0-5.5) = (less than 5-9% risk of diabetes in the next 5 years)

A1C% (6.0-6.5) = (25-50% risk of diabetes in the next 5 years)

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28
Q

Describe Type 2 Diabetes (T2DM)

A

It accounts for 90% of DM

It is caused by impaired insulin secretion and resistance

Manifests only in those who lose the ability to produce sufficient quantities of insulin to maintain normoglycemia in the face of insulin resistance

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29
Q

What are some causes of Type 2 Diabetes (T2DM)?

A

Involves the interaction of genetic and environmental factors

Genetics: certain genes have been shown to determine risk for T2DM

Environ.: excessive caloric intake, sedentary lifestyle

Aging

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30
Q

What are some risk factors for T2DM?

A

Age over 40

First-degree relative with T2DM

Member of high risk population (African, Arab, Asian, Hispanic, Indigenous, or South Asian, low socioeconomic status)

Overweight/obesity

History of prediabetes

Low HDL, high TG, HTN, smoking

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31
Q

Explain how abdominal obesity is a risk for diabetes?

A

Insulin resistance is found in most obese people (WC (male over 102cm, and female over 88cm)

The degree of obesity correlates with degree of insulin resistance

Visceral adipose tissue is even worse, and it is especially stubborn to insulin action

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32
Q

Why is insulin secretion impaired in response to food in patients with T2DM?

A

Impaired cell function (remaining cells put into overdrive and this degrades them)

A reduced stimulus from incretin hormones

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33
Q

What are the consequences of defective insulin secretion?

A

Hyperglycemia

In early stage, elevated PPG (post-prandial glucose)

In late stage, elevated FPG (fasting plasma glucose)

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34
Q

How does insulin resistance work in different organs?

A

There is reduced sensitivity yo the actions of insulklin by the target tissues (muscle, liver, adipocytes)

Skeletal muscle (primary site of resistance): Decreased glucose uptake

Liver: inability to suppress hepatic glucose production (gluconeogenesis)

Adipose tissues: Elevated fatty acids in circulation can stimulate liver glucose production, impair skeletal muscle sensitivity, and impair insulin release

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35
Q

review the Ominous Octet on page 35, to examine the many causes and effects of hyperglycemia

A
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36
Q

Are the symptoms of T2DM apparent from the get go?

A

No, T2DM is a progressive disease. This means that that insulin secretion and resistance gradually decreases over long periods of time (years)

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37
Q

What is the clinical presentation of Type 1 Diabetes (T1DM)?

A

Usually presents as acute symptoms of short duration:
Polyuria (frequent urination)
Polyphagia (frequent eating)
Polydipsia (excessive thirst)
Weight loss

Fatigue
Blurred vision
Infections

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38
Q

What is the clinical presentation of Type 2 Diabetes (T2DM)?

A

Is commonly discovered incidentally, as patients may be asymptomatic. If symptoms exist, they are non-specific:

Fatigue
Polyuria
Polydipsia
Nocturia

Due to T2DM slow progression, at time of diagnosis, the patient may have already developed complications (ex. micro/macrovasular damage)

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39
Q

Review slide 40 and 41 to study clinical features in both Type 1 and Type 2 Diabetes

A
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40
Q

Are people with Type 1 Diabetes usually obese?

A

They are usually thin, but due to general widespread obesity in the population, they may be obese (Type 1 diabetes is not making them obese)

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41
Q

What is the relationship between Type 2 Diabetes (T2DM) and children?

A

Traditionally children have not been affected by T2DM

It’s predicted that 1 in 3 kids born 2000 will develop diabetes at some point, and 1/3 of diagnoses in patients under 18 will be of T2DM

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42
Q

What is the trend of obese children in terms of their body weight in adulthood?

A

They will usually remain obese. Adults are getting more obese every generation as obese children become adults

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43
Q

What is gestational diabetes mellitus (GDM)?

A

A condition that develops during pregnancy primarily due to insulin resistance

Overall prevalence 4% (indigenous women 8-18%)

Gestational diabetes mellitus increases the risk of fetal hyperinsulinemia, heavier birth weight, higher rates of C-sections, and neonatal hypoglycemia.

Increases the risk of both mother and child eventually developing T2DM

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44
Q

What are some risk factors for gestational diabetes mellitus (GDM)?

A

All women should be screened for GDM between 24-28 weeks of pregancy

Previous GDM
Member of high-risk population
Previous delivery of macrosomic infant (heavy baby)
Age over 35
Obesity

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45
Q

Can Type 1 Diabetes (T1DM) be prevented?

A

No successful preventative interventions thus far

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46
Q

Can Type 2 Diabetes (T2DM) be prevented?

A

Yes, primarily targeting high risk individuals (IGT or obesity to prevent progression)

Methods:
Lifestyle modification

Metformin
Other Antihyperglycemic agents (Acarbose, Pioglitazone, Rosiglitazone, Orlistat, Liraglutide)

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47
Q

Is lifestyle modification effective in preventing prediabetes from advancing into T2DM?

A

Yes, intensive lifestyle modification can reduce the incidence of diabetes more than antihyperglycemics like Metformin.

The effects of lifestyle modification, even if return to previous habit for years, the incidence of diabetes is still lower vs. patients that were on antihyperglycemics alone

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48
Q

Is screening done in T1DM?

A

No, screening is not recommended due to low prevalence of T1DM and there is nothing we can do to prevent T1DM

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49
Q

Is screening important in T2DM?

A

Yes, it is important because a large number of people are undiagnosed. We use FPG and A1C as our initial screening tests

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50
Q

Review Slide 56 for details on screening guidelines for T2DM

A
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51
Q

What is a common tool used to determine risk level in diabetes?

A

CANRISK (Canadian Risk Assessment Questionnaire)

This risk assessment tool takes into consideration the following:
Patient age, sex, height, BMI, WC, physical activity, HTN, hyperglycaemia during illness or pregnancy, family history, ethnic group, and education

This test helps identify which patients should be referred to physicians for further work-up

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52
Q

What are some test results that result in a diabetes diagnosis?

A

FPG more than 7.0mmol/L

A1C more than 6.5%

2hPG(75mg) more than 11.1mmol/L

Random PG more than 11.1mmol/L

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53
Q

Is FPG more convenient vs A1C?

A

No, FPG requires fasting (fasting plasma glucose), while a blood sample for A1C can be administered at anytime without respect to meals

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54
Q

What are some advantages and disadvantages of FPG (fasting plasma glucose)?

A

Advantages:
Established standard of reliability
Fast and easy

Disadvantages:
Inconvenient
Less sensitive than 2hrPG(75mg)

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55
Q

What are some advantages and disadvantages of A1C?

A

Advantages:
Convenient
Better predictor of CVD
No day-to-day variability

Disadvantages:
Cost
Results invalid in some medical conditions (anemia, hemoglobinopathies)
Altered by ethnicity and aging
Do not use in children, gestational diabetes mellitus, and suspected T1DM

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56
Q

What are some of the advantages and disadvantages of 2hrPG(75mg)?

A

Advantages:
Like FPG, 2hrPG(75mg) is an established standard

Disadvantages:
Inconvenient (need to wait 2h before patient can test themselves
Taste
Cost

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57
Q

What are some complications of diabetes that first come to patients when they are first told they have diabetes?

A

Patients often think about end stage outcomes of poorly managed diabetes.

Amputation, and kidney failure/dialysis are some common worries

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58
Q

What are some general treatment goals for diabetes?

A
  1. Be symptom free (avoid hyper or hypoglycaemia)
  2. Achieve personalized target glucose levels
  3. Address modifiable CV risk factors
  4. Prevent or slow the progression of micro vascular complications
  5. Empowerment to self-manage condition
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59
Q

How can glucose control be adequately monitored?

A

This is an essential component of diabetes management

Blood glucose lab evaluations

Hemoglobin A1C

Capillary blood glucose (cBG)

Continuous glucose monitoring (CGM):
Intermittently scanned CGGM (isCGM), ex. Libre
Real-time CGM (rtCGM), ex. Dexcom G6

Ketone testing (urine or blood)

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60
Q

What is the significance of glycosylated hemoglobin?

A

The percentage of glycosylated hemoglobin A is represented by A1C. This glycosylation reaction is irreversible, so glycosylated hemoglobin remains in the blood supply until they breakdown in 3 month

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61
Q

How often should a A1C testing be preformed on a patient?

A

Should be checked at least every 3 months. You may feel like you are okay, but could be silently at high risk of developing diabetes

Normal A1C levels are 4-6%

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62
Q

What are some general conditions that could affect A1C levels?

A

Any condition that can effect RBC, will change their A1C values.

ASA and Vitamin C and E can decrease A1C

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63
Q

Review slide 68 for more details on how different conditions can effect A1C

A
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64
Q

What are some A1C targets?

A

Selected adults with T2DM who have the potential to return to normoglycemia (under 6.0%)

Adults with T2DM to reduce CKD and retinopathy if at low risk for hypoglycaemia( 6.0-6.5%)

Most adults with T1DM or T2DM (6.5-7.0%)

Functionally dependent people (7.1-8.0%)

Recurrent severe hypoglycaemia, limited life expectancy, and frail elderly and/or with dementia (7.1-8.5%)

Avoid any A1C target above 8.5%

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65
Q

What is the A1C target for most diabetes patients?

A

7.0%

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66
Q

What are the FPG and 2hrPG(75mg) targets to achieve an A1C score below 7.0?

A

FPG: 4.0-7.0mmol/L (4.0-6.0 is more aggressive)

2hrPG(75mg): 5.0-10.0mmol/L (5.0-8.0 is aggressive)

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67
Q

Why do HCPs like to bring A1C below 7.0?

A

Great decreases in retinopathy (-63%), neuropathy (-60%), and microalbuminuria (-39%).

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68
Q

Is intensive treatment that results in A1C being depressed below an A1C of 7.0% worth it?

A

Yes, although this increases risk of hypoglycaemia, overall reductions in other diseases associated with diabetes are well worth it

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69
Q

Do the effects of intensive A1C depression persist?

A

Although A1C may return to a level above 7.0 in a shorter period of time (1 year), risk reductions persist for over a decade

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70
Q

If reducing A1C to below 7.0% presents great benefits, why is the A1C target not set lower?

A

In a trial where the A1C target was set to 6.0%, there were more deaths than usual. This trial was stopped early due to the number of deaths

Increase in mortality is likely due to increased severe hypoglycaemia or other less understood reasons

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71
Q

What are some limitations with A1C?

A

A1C is an average value, we cannot detect lows and highs in blood glucose levels

A1C cannot tell us changes in the day-to-day, because it is an average value of 3 months of glycosylation

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72
Q

What are capillary blood glucose monitors?

A

These are the standard glucose monitors

They determine the glucose level in a capillary blood via a finger stick

This monitor can tell a patient their blood glucose level at a particular point in time (immediate feedback)

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73
Q

What do patients need to know about CBGs (capillary blood glucose monitors)?

A

How to perform a CBG

How often and when to perform a CBG (before or after meals)

The meaning of various blood glucose levels:
FPG - reflects glucose derived from hepatic production (gluconeogenesis)
PPG - how meals effect glucose

How behaviour and actions affect CBG results (interpretation of trends in blood glucose)

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74
Q

How many times should diabetes patients check their blood sugar?

A

At least as many. Times as insulin is injected.

Test before injecting insulin to determine required insulin quanity.

Optional: Test 2 hours after meal to see the efficacy of insulin (lower blood sugar)

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75
Q

DO diabetes patients need to test themselves regularly if they are not on insulin or have stable blood sugar levels?

A

No, there is no point plus it is expensive to test everyday for no reason

This is why the Sask Drug Plan only covers for 200 strips in diabetic patients in this category

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76
Q

How do intermittently scanned CGM monitors work?

A

They measure glucose levels in the subcutaneous interstitial fluid via a sensor that is inserted into the skin. These monitors can help identify when a patient goes into either hyper or hypoglycaemia

Ex. Libre

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77
Q

What is glucose lag?

A

Intermittently scanning CGMs measure blood sugar in subcutaneous tissue. Changes in actual blood sugar can take up to 5-15 minutes to be reflected in subcutaneous tissue.

This is a minor issue, focus on the overall trend

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78
Q

What is the difference between intermittently scanning CGMs (isCGM) and real-time continuous glucose CGMs (rtCGM)?

A

rtCGMs like isCGMs detect glucose levels in the subcutaneous tissues, instead of blood glucose directly

The main difference is the continuous data visibility 24/7 offered by rtCGMs. rtCGMs punch out data every 5 minutes vs. every 15 min in isCGMs

rtCGMs can be applied on back of arms, abdomen, buttocks while isCGMs can only be applied on the back of arm.

Ex. Dexcom G6

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79
Q

What is Time in Range (TIR)?

A

Newer CGMs continuously check glucose levels, diabetes patients can monitor the time they spend within their target blood glucose range

Most diabetes patients should aim to be within TIR for 70% of the time (17h/24h)

There is a shift away from FPG and PPG and towards using TIR

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80
Q

What is the exact relationship between TIR and A1C?

A

Every 10% (2.4h/24h) increase in TIR = 0.5% decrease in A1C

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81
Q

What is the relevance of ketones in diabetes?

A

Ketones are formed as a byproduct of fat breakdown. Fats are broken down because the body is unable to pull glucose from the blood. Increased ketones can indicate cell starvation and poorly managed diabetes

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82
Q

What are the two main approaches to achieving glucose targets?

A

Non-pharmacological

Pharmacological

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83
Q

What is the non-pharmacological treatment for Diabetes?

A

Diet modification is the cornerstone of diabetes care. It can be 1st line + exercise for T2DM

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84
Q

How does nutritional education play out in T1DM and T2DM treatment?

A

T1DM: Nutritional education is vital to understand the relationship between carbohydrates, insulin, and blood glucose

T1DM and T2DM: Nutritional education should focus on understanding the relationship between food and its effects on body weight, blood glucose, BP, and lipids (CV risk)

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85
Q

Is there a standardized diabetic diet?

A

No, there is nor such thing as a diabetic diet

Each patient should meet with a dietitian if possible to individualize diet based on patient goals and preferences(be mindful of the cultural importance of food)

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86
Q

What are some diets that are popular in diabetes control?

A

Mediterranean

Vegan/ vegetarian

Low CHO (50-130g/d)

DASH (Dietary Approaches to Stop Hypertension)

Intermittent Fasting

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87
Q

Is all weight loss beneficial in terms of health?

A

5-10% weight loss has shown to provide health benefits, but weight should only be reduced if it poses a health benefit (do not be underweight)

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88
Q

What is the place of carbohydrates in the diet of a diabetes patient?

A

Generally people should consume 45-60% of their diet from carbohydrates

In patients that use insulin, know the relationship between carbohydrates, insulin, and blood glucose is paramount. Ensure diabetes patients who are on insulin, are counting carbohydrates to accurately adjust insulin doses

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89
Q

What is glycemic index, and is a smaller number better?

A

Glycemic Index is a measure of how quickly a given piece food will elevate blood glucose levels. More simple sugars=higher glycemic index

A smaller Glycemic Index value suggests that the piece of food in question delivers glucose over a longer period of time (shorter peak). This is reduces the risk of being hyperglycemic while on insulin (if not adjusting dose)

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90
Q

Do whole fruits have a higher glycemic index vs. Fruit juice?

A

No, fruit juice has a higher glycemic index vs. whole fruits

Fruit juice will increase blood glucose much more faster and will have a higher peak glucose blood glucose concentration

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91
Q

What groups of food have little or no carbohydrate?

A

Meat & Alternative (except for some beans)

Vegetables (except squash, parsnips, and peas)

Fats

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92
Q

What is the utility of fibre in diabetic patients?

A

Soluble fibre slows gastric emptying and delays sugar absorption in small intestine (it is a type of carbohydrate that cannot be digested, so subtract from total carbohydrates)

For patients 19-50, 25g/d(women), and 38g/d (men)

For patients over 50, 21g/d(women), and 30g/d(men)

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93
Q

Review Slides 118-120 to look at some diets followed by diabetes patients

A
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94
Q

What are some definitions for servings for different groups of food?

A

Grains & Starches, Fruits: 1 serving = size of patient’s fist

Meat & Alternatives: Size of the patient’s palm

Vegetable: As much as the patient can hold in their two hands

Fats: Limit fat to a amount the size of your thumb

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95
Q

Can practicing Muslim diabetes patients follow Ramadan safely?

A

Depends on their individual risk factors

Guidelines encourage consultation with dieticians/diabetes educators two months before Ramadan

Advise T1DM patients across the board to not fast (it is their choice ultimately)

T2DM patients with the following are advised to fast during Ramadan with medical advise:
Well controlled diabetes
Treated with lifestyle modifications alone, or with antihyperglycemics, or basal insulin (not bolus insulin) in otherwise healthy individuals

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96
Q

What are some nutritional tips that can help control blood sugar?

A

Consistent spacing of meals

Snacking between meals could help with hyperglycemia

Sugar is acceptable up to 10% of daily energy intake

Coffee is fine in moderation

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97
Q

What is the effect of alcohol on diabetes patients?

A

With people with T1DM, or with T2DM on insulin or sulfonylureas; alcohol can delay hypoglycaemia

Hypoglycaemia can persist for up to 24h after the last drink

It is important that diabetes patients test regularly when they are drinking alcohol

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98
Q

What is the effect of physical activity on diabetes patients?

A

Physical activity increases cardio/respiratory fitness and can decrease insulin resistance

Physical activity has been proven to improve A1C in T2DM and T1DM in kids, but evidence is less clear for T1DM in adults

Exercise still reduces risk of CVD and stroke even if it does not directly reduce diabetes markers

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99
Q

What are the recommendations for exercise in diabetes patients?

A

More than 150 min of moderate to vigorous intensity aerobic exercise/week

Spread over more than 3 days/week

No more than 2 consecutive days of no activity

Resistance training more than 2 times/week

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100
Q

Should diabetes start the recommended level of exercise immediately after diagnosis?

A

No, MD has to assess for conditions that can predispose to injury (neuropathy, retinopathy, CAD)

Ensure patient can tolerate exercise from a cardiovascular aspect (perform ECG)

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101
Q

What is the effect of exercise on blood glucose?

A

Low-moderate intensity:
Decreases blood glucose during and after due to increased insulin sensitivity (decreased insulin resistance lasts for up to 48h)

Very intense exercise:
Increases blood glucose during and after due to increased glucose demand

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102
Q

What are some tips for exercising in patients with T1DM?

A

The goal is to maintain safety (minimize risk of hypoglycemia)

Strategies:
INject insulin at a non-exercise site
Consume extra carbohydrates before/during/after exercise

Decrease bolus insulin that is closest to time of actvity
OR
Decrease basal insulin overnight by 20%

Perform resistance training before aerobic exercise

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103
Q

What should T2DM patients do when they have high blood glucose and are about to start exercising?

A

It is okay for T2DM patients to exercise on high blood glucose as long as there are no signs of dehydration and patient feels fine

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104
Q

What should a T1DM patient do if they wanted to exercise, but their blood glucose is high?

A

If blood sugar is above 16.7mmol/L + feel unwell:
Check ketones and postpone vigorous exercise until insulin is given and ketones are resolves

If sugar is high, but feel fine and no ketones, go ahead and exercise

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105
Q

What is insulin?

A

It is a hormone secreted from pancreatic beta-cells to help regulate blood glucose

In the body, proinsulin is cleaved into insulin and C-peptide

Commercially available products only contain insulin

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106
Q

What is the difference between basal and bolus release of insulin?

A

Basal release:
Beta cells secrete small amounts of insulin throughout the day (maintain baseload)

Bolus release:
At mealtime, insulin is rapidly released in response to food (increases secretion at times of increased glucose)

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107
Q

What do the onset, peak, and duration of rapid acting insulin analogues (RAIA) look like?

A

RAIA onset:
10-15 min

RAIA peak:
1-2 hours

RAIA duration:
3-4 hours

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108
Q

What do the onset, peak, and duration of short-acting insulin analogues look like?

A

Short acting onset:
30min

Short acting peak:
2-3 hours

Short acting duration:
6.5 hours

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109
Q

What does the onset, peak, and duration of Insulin regular U-500 look like?

A

U-500 onset:
15 min

U-500 peak:
4-8 hours

U-500 duration:
17-24 hours

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110
Q

What makes rapid acting insulin analogues (RAIA) have a short onset, high peak, and short duration of effect?

A

They have modifications to the basic Humulin Insulin. These modifications allow them to have more rapid absorption vs. Short acting insulins. RAIAs also more closely mimic endogenous insulin release

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111
Q

What are some advantages of RAIA over short acting insulin?

A

More rapid absorption

Quicker peak

Shorter duration of action

More convienent:
Can be taken 0-15 min before a mean or within 15 minutes of eating, short acting is 30-45 min (more flexibility on what patient want’s to eat, can adjust insulin dose appropriately)

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112
Q

How is Insulin regular U-500 administered?

A

It is a very concentrated form of insulin (extreme caution is required to avoid inadvertent overdose)

Given 2-3 times per week

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113
Q

What does the onset, peak, and duration of intermediate-acting insulin look like?

A

Intermediate Onset: 1-3h

Intermediate Peak 5-8h

Intermediate duration: up to 18h

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114
Q

What does the onset, peak, and duration of long-acting insulins look like?

A

long-acting onset: 90 min

Long-acting peak: no real peak, very flat curve

Long-acting duration: (24-42h)

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115
Q

Describe intermediate-acting insulins

A

Administered once or twice daily to provide a basal amount of insulin

Appear cloudy (need to resuspend by hand-rolling or inverting 10x)

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116
Q

Describe long-acting insulin?

A

3 main versions (glargine, detemir, and degludec). All have amino acid modifications to help them achieve long durations of effect

Glargine: forms micropreciptates which slowly dissolve, 24-30h duration of effect

Detemir: Prolonged duration of effect due to hexamer stability

Degludec: longest duration of effect (42h)

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117
Q

What are the advantages of long acting insulin analogues (LAIAs) vs. intermediate acting insulin?

A

They are “peak less” (long duration of effect)

More consistent blood glucose

Less hypoglycaemia due to consistent reduction in blood glucose (less variable)

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118
Q

When switching between long acting insulin analogues (LAIAs), what are some dosing considerations?

A

Maintain the same dose unless patient is moving from the following:

Reduce new insulin dose by 20% when moving from the following:

Insulin glargine 300u/mL (Toujeo)
Insulin detemir (Levemir) BID
Insulin NPH BID

*Insulin glargine 100u/mL (Lantas), but only when switching to Degludec (Tresiba)

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119
Q

What are the main types of insulin delivery devices commonly used by patients?

A

Syringes and vials (least popular, but rational choice)

Insulin pens

Insulin pumps

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120
Q

What are some advantages of syringes as an insulin delivery device?

A

Traditional method of insulin delivery, but some prefer it due to the following reasons:

Least expensive
Used to it (familiarity)
Prefer less injections and want to combine some insulin sin same syringes

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121
Q

What does the gauge number mean for needles?

A

Higher gauge=thinner needle

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122
Q

What are some advantages of insulin pens?

A

Insulin pens have largely supplanted vials/syringes for the following reasons:

Portable/convenient/easier to use
Advantageous if dexterity/visually impaired
Allows for precision dosing (easier to administer an accurate dose)

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123
Q

What are insulin pumps?

A

Also known as a continuous subcutaneous insulin infusion (CSII)

It is a small computerized devices that delivers insulin continuously 24h a day, but can also increase release rate when a bolus release is needed

The pump is worn on the outside of the body and only delivers RAIAs via a tube which is attached to a cannula placed under the skin (changed every 3 days)

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124
Q

What are the advantages of insulin pumps?

A

Patient/guardians should be motivated and able to understand what is entailed before deciding on using a insulin pump

Consider insulin pumps for the following patients:
Poorly controlled with optimized injections
Significant glucose variability
Frequent severe hypoglycaemia
Pregnancy

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125
Q

What is the SK Insulin Pump Program?

A

For T1DM patients, 1 pump is covered every 5 years (up to $6300)

Pump supplies are covered for initial trial period (3 months)

Pump supplies are only further covered if patient is under Sask Income Support or SAIL program

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126
Q

What is a closed loop system in terms of glucose management?

A

This is an integrated insulin pump and CGM system that automatically adjusts insulin in response to elevation in blood sugar.

A closed loop system can mimic the pancreas (artificial pancreas)

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127
Q

What are some adverse effects of insulin?

A

Hypoglycaemia (Most common AE)

Weight gain:
Promoted glucose uptake by target cells = increased nutrition

Insulin is also a anabolic hormones that promotes energy storage via glycogen, protein, and lipid synthesis (localized fat hypertrophy)

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128
Q

What are some factors that affect insulin absorption?

A

Exercise of injected area = increased

Massage = increased

HIgher temperature = increased

Depth of insulin IV>IM>SC

Lipohypertrophy = decreased

Reduced renal function = decreased

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129
Q

What is the recommended injection technique for insulin?

A

Wash your hands

Alcohol swab cartridge/vial (don’t need to wipe injection area)

Rotate injections systematically within the same anatomical region (impact on absorption rate and lipohypertrophy)

Avoid moles, scars, and other blemishes

Use a quick, smooth movement

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130
Q

What are the preferred injection sites?

A

Around the belly button

Side of upper thigh

Love handle region (above buttocks)

Under arm region

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131
Q

Review slides 171-173 for rotating sites

A
132
Q

What is proper technique for injecting insulin with a syringe?

A
  1. Pull in hair
  2. Push air into the bottle
  3. Pull in and push out a little insulin to remove air bubbles
  4. Pull your exact dose of insulin into the syringe

Inject with or without skin lift, but inject at 90* regardless

After pushing the plunger, leave the syringe in place for 10 seconds

After removing syringe, the skin should look normal

133
Q

What is the proper technique for delivering insulin via an insulin pen?

A
  1. Wash hands (remove the pen cap)
  2. Wipe pen tip with alcohol swab
  3. Safety test (priming with 2 units)
  4. Dial up amount of insulin required
  5. Inject ideally at 90*
  6. Count until 10 and then remove needle
134
Q

How should insulin be stored?

A

Unopened: fridge

In-use: room temperature (discard after 28 days, degludec can last up to 56 days)

Avoid freezing, extreme heat, or direct sunlight

135
Q

What insulin mixtures are stable?

A

R+NPH (can be pre-mixed and stored together)

RAIA+NPH: (may mix together, but cannot be stored for future use)

LAIA (cannot mix in the same syringe as any other insulins)

136
Q

What are some typical insulin doses in T1DM?

A

Initial dose: 0.5-0.6u/kg

Honeymoon phase: 0.1-0.4u/kg

Ketosis or acute illness: 0.5-1.0u/kg

137
Q

What are some typical insulin doses in T2DM?

A

Initial dose: 0.1u/kg

With insulin resistance: 2.5u/kg

138
Q

What is the importance of insulin T1DM?

A

Insulin is necessary, and it is ideally delivered in a manner that mimics normal physiologic insulin secretion

MDI (multiple daily injections = (3 bolus + 1 basal dose)/day)

139
Q

What is the distribution of insulin delivered in basal and bolus doses?

A

Basal: 40-50%

Bolus: 50-60%

140
Q

Does the exact regimen of insulin change over time?

A

Yes, it can change depending on patient age, goals, general health, glucose levels, physical activity

Insulin adjustment is an art and science, and is always changing

141
Q

What is the carbohydrate to insulin ration (C:I)?

A

This ration is used to estimate how many grams of carbohydrates each unit of meal-time insulin will cover

Typical C:I is 15:1, therefore 15g of carbs is taken care of by 1g of insulin

142
Q

What is correction factor (CF) in terms of insulin dose adjustment?

A

Correction factor (CF) can help bring down high blood glucose detected before meals (allows patient to take care of high blood sugar and future increase in blood sugar after eating a meal)

CF=100/total daily dose

143
Q

What is the Somogyi Effect?

A

Unrecognized nocturnal hypoglycemia (under 4mmol/L) that patient sleeps through

Likely due to excess or ill-timed insulin

144
Q

What is the Dawn Phenomenon?

A

This is fasting hyperglycaemia that is the result of growth hormones, cortisol, glucagon being released in the early morning

Avoid carbohydrates after dinner/eat earlier
Be active after dinner

145
Q

What are some general rules for adjusting doses?

A

Fix the low readings first (hypoglycemia)

Generally adjust by 1-2 units at a time (1u of insulin can reduce blood glucose can reduce blood glucose 2-3 mmol/L

ONly adjust 1 dose at a time, begin with correcting the first problem blood glucose of the day

Make dose adjustments every few days based on glucose trends, not just single readings

146
Q

What is the mechanism of action for Metformin?

A

Not fully understood, but it reduces hepatic glucose production and enhances insulin sensitivity

147
Q

What are some doses for Metformin?

A

Start at 250-500mg OD

Titration up by 500mg weekly if no GI side effects

Desired usual dose: 850-1000mg BID, max dose = 850mg TID

148
Q

What is the efficacy of Metformin?

A

Reduces A1C% by 1-1.5% in most patients (up to 2% in patients with especially high A1C (9%))

Metformin also decreases triglycerides, LDL (-8 to -15%) and slightly increases HDL (+2%)

149
Q

What are some drug interactions with Metformin?

A

Cimetidine (competes for renal tubular secretion, increases circulating Metformin)

Dolutegravir (can increase Metformin concentration)

Alcohol (potentiates Metformin’s effect on lactate metabolism, enhanced hypoglycemic effect)

Contrast media (continues for 48h after imaging)

150
Q

What are the adverse effects of Metformin?

A

GI symptoms: Diarrhea, nausea, abdominal discomfort (30% will experience, and about 5% will d/c)

Less common:
Metallic taste
Vitamin B12 deficiency with long-term use
Hypoglycemia (rare in mono therapy)

151
Q

What is a rare medical emergency associated with Metformin use?

A

Lactic acidosis: Decrease in arterial pH and an accumulation of serum lactate (medical emergency)

Accumulation occurs due to metformin-mediated inhibition of the conversion of lactate into glucose. This condition is worsened in patients with CKD as they are unable to clear lactate effectively

152
Q

How are metformin doses adjusted to patients with CKD?

A

eGFR (45-59mL/min): 1500mg/d

eGFR (30-44mL/min): 1000mg/d

eGFR (under 30mL/min): do not start, but continue 500mg OD

153
Q

What are some risk factors for lactic acidosis?

A

History of lactic acidosis

Severe liver disease

Alcohol abuse

Radiologic procedures (contrast dye)

Acute illness (severe infection and trauma)

Severe dehydration

154
Q

What is the mechanism of action for sulfonylureas?

A

They enhance the secretin of insulin by binding to sulfonylurea receptors in the beta cells of the pancreas.

Once binded to the beta cells, it promotes the closure of K+ channels and the opening of Ca2+ channels. This in turn stimulates insulin secretion

155
Q

What are some examples of sulfonylureas?

A

Glyburide, gliclazide, glimepiride

156
Q

What is the dosing of different sulfonylureas?

A

Glyburide and Gliclazide MR are the most prescribed sulfonylureas in Sask (bc they are coved by the drug plan)

Glyburide (5-20mg/d), d/c after eGFR falls below 60mL/min

Gliclazide MR (30-120mg OD), d/c after eGFR falls below 30mL/min

157
Q

What is the efficacy of sulfonyureas ?

A

A1C reduction from 1-1.5%

Can titration up to regular dose after 2 weeks

Effective at 1/2 of max dose, but max effective dose is about 60-70% of max dose

Need to adjust dose in CKD patients

158
Q

What is the impact of sulfonylureas on reducing CV risk?

A

Do not appear to cause harm, but also no benefit (neutral)

159
Q

What are some adverse effects associated with sulfonylureas?

A

Hypoglycemia (2-30%)

Glyburide is on the BEERS list of agents to avoid in elderly patients due to its risk of causing hypoglycemia

Weight gain (2kg)

Less frequent:
Nausea, skin reaction, rash, photosensitivity

160
Q

Are sulfonylureas safe for use in pregnancy?

A

Glyburide is the only sulfonylureas that does not cross the placenta (desirable for fetal health)

161
Q

What is the mechanism of action for repaglinide (Meglitinides)?

A

Repaglinide was bound to site adjacent to the sulfonylureas receptor, resulting in stimulation of the secretion of insulin from the pancreas

162
Q

What is the efficacy of Repaglinide?

A

Reduced A1C by 1-1.5%

Works primarily to decrease PPG, is intended to be taken before meals to improve their meal-induced and secretion

163
Q

What are some dosing guidelines for repaglinide?

A

A1C under 8%: initiate at 0.5mg before each meal and titrate up

A1C over 8%: Initiate at 1-2mg before each meal and titrate up

Max dose: 4mg before each meal (max dose 16mg/d)

It needs to be administered shortly after a meal due to sort duration of action

164
Q

What are some adverse effects associated with repaglinide?

A

Hypoglycemia (especially when combined with other agents)

Weight gain: 0.3-1kg

165
Q

What are some precautions drug interactions that are associated with repaglinide?

A

CYP450 (precaution in patients with moderate hepatic impairment)

Increased repaglinide with:
CYP 3A4 inhibitors (clarithromycin, grapefruit, azoles)

166
Q

What is the mechanism of action for acarbose (alpha-glucosidase inhibitors)?

A

a-Glucosidase enzymes are responsible for breaking down polysaccharides into glucose. By inhibiting a-Glucosidase enzymes, we reduce the about of glucose being absorbed

Net effect is on post-prandial glucose, rather than fasting glucose unlike most antihyperglycemics

167
Q

What is the efficacy of acarbose?

A

Can reduce A1C by 0.5-0.8% (less than others)

168
Q

What are some doses for acarbose?

A

Initial 25-50mg OD, titrate up every couple weeks to 50mg TID

Assess for efficacy every 4-8 weeks to a max dose of 100mg TID

Take with the first bite of each main meal

169
Q

What are some adverse effects associated with acarbose?

A

Flatulence (40-80%) and Diarrhea (30%)

This is the main reason why acarbose is an unpopular antihyperglycemic agent

Negligible hypoglycemia risk

Weight neutral

170
Q

In what patient populations should caution be used when using acarbose?

A

Those with IBD or GI conditions

eGFR under 25mL/min and severe liver disease

171
Q

What is the mechanism of action for Thiazolidinediones (Rosiglitazone and Pioglitazone)?

A

They bind to PPAR-y receptors which are primarily found in adipose tissue. Their activation alters genes that influence glucose and lipid metabolism.

Due to activation by either “Rosi” or “Pio”, insulin sensitivity is enhanced at muscle, liver, and fat tissues

172
Q

What is the efficacy of Thiazolidinediones (Rosiglitazone and Posiglitazone)?

A

They reduce A1C by 1-1.5%

Effects on TG: “Pio” decreases by 10-20%, “Rosi” is neutral

Effects on LDL: “Rosi” increase LDL by 5-15%, “Pio” is neutral

Effects on HDL: Both may increase HDL to some degree

173
Q

What is the dosing for Thiazolidinediones (Rosiglitazone and Pioglitazone)?

A

“Rosi”: initiate at 2-4mg ODD, may increase to 4mg BID

“Pio”: initiate at 15mg OD, titrate up to 30-45mg OD

Give 4-8 weeks before making dose adjustments

Larger people need a larger dose

Caution in patients with eGFR under 60mL/min (no dose adjustment required)

174
Q

What are some drug interactions associated with Thiazolidinediones (Rosiglitazone and Pioglitazone)?

A

Metabolized by CYP 2C8

175
Q

What are some common adverse effects associated with Thiazolidinediones (Rosiglitazone and Pioglitazone)?

A

Peripheral edema (5%), and jumps to 15% when on insulin (do not use with insulin)

Weight gain (2.5-4.8kg), increased distal fractures in post-menopausal women

Increased distal fractures in post menopausal women

176
Q

What is the current opinion on the use of Thiazolidinediones (Rosiglitazone and Pioglitazone) in terms of CV risk?

A

Due to mixed results, Rosiglitazone has restricted access

177
Q

What are the two incretin-based therapies?

A

GLP-1 receptor agonists

DPP-4 Inhibitors

178
Q

Describe incretin hormones

A

GLP-1 and GIP are secreted from the gut in response to ingestion of nutrients

Main role is to augment insulin secretion

People with T2DM have a reduced incretin effect

179
Q

What happens when the GLP-1 receptor is activated?

A

Potent inhibition of gastric emptying

Potent inhibition of glucagon secretion

Reduction of food intake and body weight

180
Q

What is the mechanism of action for DPP4-inhibition?

A

Block the enzyme DPP4 which rapidly hydrolyzes incretins, thus enhancing the action of endogenous incretins (promoting increased insulin release)

181
Q

What is the efficacy of DPP4-inhibitors?

A

Reduces A1C by 0.7% (less than a lot of other agents, it is more gentle so preferred by the elderly)

Works quickly, see effects within a couple of weeks

182
Q

What are some adverse effects associated with DPP4 inhibitors?

A

Overall, well tolerated medications (headache, nasopharyngitis, URTI)

No hypoglycemia on their own

Weight neutral

183
Q

What are some drug interactions with DPP4 inhibitors?

A

When combined with sulfonylureas or insulin, it may increase the risk of hypoglycemia

Avoid with GLP1RA (similar MOA and increased risk of pancreatitis)

184
Q

What is the mechanism of action for GLP1RAs?

A

They stimulate insulin secretion in a glucose-dependent manner, reduces glucagon, slow district emptying, and increase satiety

185
Q

How are GLP1RAs safely stored?

A

At the pharmacy or at home and not in use: in the fridge

When at home and in use: room temperature or fridge

186
Q

What are the short-acting GLP1RAs?

A

Exenatide

Lixisenatide

187
Q

What is the dosing for short-acting GLP1RAs?

A

Exenatide: 5mcg BID sc x1 month, then 10mcg BID

Lixisenatide: 10mcg OD sc x 14 days, then 20mcg OD

188
Q

What are the long-acting GLP1RAs?

A

Liraglutide

Exenatide QW

Dulaglutide

Semaglutide

189
Q

What is the dosing for long-acting GLP1RAs?

A

Liraglutide: 0.6mg OD x 1 week, then 1.2-1.8mg OD

Exenatide QW: 2mg sc every week

Dulaglutide: o.75mg sc every week (can increase to. 1.5mg every week)

Semaglutide: 0.25mg sc weekly, increase to 0.5mg after 4 weeks then 1mg

190
Q

How is the bioavailability of oral Semaglutide increased (only GLP1RA that comes in an oral formulation)?

A

It is co-formulated with SNAC (forms a bubble around Semaglutide, preventing degradation from stomach acid) only 1% makes the journey

191
Q

What are some renal dosing considerations for GLP1RAs?

A

Dulaglutide: Caution eGFR under 15mL/min

Liraglutide: Caution eGFR under 15mL/min

Semaglutide SC: Caution eGFR under 15mL/min

Semaglutide po: Caution eGFR under 30mL/min

Exenatide QW and Exenatide: Caution under 30mL/min

Lixisenatide: Caution under eGFR 30mL/min

192
Q

What is the efficacy of GLP1RAs?

A

Reduce A1C by 1-1.5% (Semaglutide sc seems to be more potent than Dulaglutide)

Long-acting GLPs are more potent (more effect on FPG) vs. Short-acting (more effect on PPG)

193
Q

What are some adverse effects associated with GLP1RAs?

A

N/V/D (up to 40%), especially nausea (20-50%)

Nausea and vomiting are generally mild and transient. They will typically resolve after 4-8 weeks

194
Q

What are some tips to minimize nausea?

A

Tell patients what to expect

Eat smaller portions and slowly

Titrate slowly (stay on low dose until nausea improves)

Avoid fatty, spicy, and high fiber foods

195
Q

Is there a concern for cancer in GLP1RA use?

A

Rodents showed increased risk for people with a family history of medullary thyroid cancer (MEN2)

This is a minor concern, but it is contraindicated in humans if they have family history for MEN2

196
Q

What is the effect of GLP1RAs on weight?

A

GLP1RAs cause significantly more weight loss vs. other antihyperglycemics (average loss 3kg)

Semaglutide (ozempic) reduced weight by 6.5kg

GLP1RAs slow gastric emptying and cause a sense of satiety. This results in reduced food intake and weight loss

197
Q

What are some drug interactions with GLP1RAs?

A

GLP1RAs decrease gastric emptying, so any drugs that require rapidGI absorption, space these oral agent out (1 hour before taking GLP1RA)

Ex. Oral contraceptives, antibiotics, and narrow TI drugs

198
Q

How do GLP1RAs have cardio protective and renal benefits?

A

Most likely due a combination of metabolic, CV, and anti-inflammatory effects

199
Q

What is the mechanism of action for SGLT2 inhibitors?

A

SGLT2 is a high capacity transporter that is responsible for glucose reabsoprtion from the glomerular filtrate

By inhibiting this transporter, we effectively limit how much glucose is reabsorbed

They are insulin-independent, therefore no chance for hypoglycemia

200
Q

What is the efficacy of SGLT2 inhibitors?

A

Reduce A1C by 0.5-0.8%

Works on both FPG and PPG

Require functioning nephrons to reduce glucose (eGFR above 45). SGLT2 inhibitors also have cardio renal protection until eGFR above 25mL/min)

201
Q

What are some kidney related effects associated with starting SGLT inhibitors?

A

When initiating, SGLT2 inhibitors can cause a very early decrease in kidney function (about 5mL/min decrease in eGFR)

This is not kidney damage, but if eGFR decreases by 30% (lower dose or stop and investigate CKD)

202
Q

What are some adverse effects associated with SGLT2 inhibitors?

A

Increased urination and thirst

Mycotic genital infections (rinse and wipe after urination)

203
Q

What are some contraindications for SGLT2 inhibitors?

A

Dehydration potential for patients that are also have the following apply to them:
Elderly

Loop diuretics

Low SBP

CKD

ACEi/ARB use

204
Q

Are patients on SGLT2 inhibitors cause an increased risk for diabetic ketoacidosis (DKA)?

A

Rare, but it can be serious. Withhold SGLT2 inhibitors if patient has developed diabetic ketoacidosis.

Diabetic ketoacidosis is characterized by the following:

Difficulty breathing

Extreme thirst

N/V

Abdominal discomfort

Confusion

205
Q

Review slide 260 for a great treatment algorithm for concurrent diuretic and SGLT2 inhibitors use

A
206
Q

What are some examples of SGLT2 inhibitors?

A

End with the suffix (-glifozin)

Dapaglifozin

Canaglifozin

Empaglifozin

207
Q

What is the relationship between Canaglifozin and amputations?

A

Occur primarily in those with prior amputations, high A1C, severe neuropathy

208
Q

What is the relationship between Canaglifozin and bone fracture?

A

Only increased risk in patients who were already at risk for fractures

Older adults with high fracture risk, fall risk, and hydration status

209
Q

What is Fournier’s gangrene?

A

Very rare reaction to SGLT inhibitors

Characterized by pain, swelling, tenderness in the genital region

210
Q

What is the effect of SGLT2 inhibitors on CV risk?

A

They all lowered risk and showed beneficial effects to CV and renal outcomes

211
Q

What is the effect of SGLT2 inhibitors on renal risk factors?

A

In multiple studies, SGLT2 inhibitors all show reduced risk

212
Q

What is the the value of SGLT2 inhibitors on heart failure?

A

SGLTis showed reduction in hospitalization for heart failure

Dapa is the only SGLT2i that is covered by the SK formulary for the treatment of heart failure

213
Q

How do SGLT2 inhibitors provide cardio protective and renal benefits?

A

We aren’t completely sure, but we have a few ideas:

They induce natriuesis and glucosuria, which lowers pre-load

Decrease BP

Stimulates erthyropoietin release = more RBC = more oxygen = heart beats works less hard to deliver same amount of O2

Decreases oxidative stress and local inflammation

214
Q

What are the cardio renal benefits of SGLT2i use in associated diseases?

A

For secondary CV prevention: Empaglifozin and Canaglifozin reduce MACE (Major adverse CV events)

In patients with HF: SGLTi decrease hospitalizations in heart failure and death

In patients with CKD: SGLTi decrease cardio renal outcomes

215
Q

What are some barriers to insulin for patients?

A

More complex dosing and monitoring

Sense of failure

Fear of hypoglycemia

Needle phobia (better now with weekly injections)

Fear/denial of disease progresssion

MIsconceptions

216
Q

What are some barriers to insulin for HCPs?

A

More complex

Fear of patient getting hypoglycemic

Patient’s cognitive ability to manage insulin effectively

217
Q

How is insulin initiated into a patient’s therapy profile?

A
  1. Basal insulin + antihyperglycemic agent:
    Usually added to existing antihyperglycemic agent

(Started at 10U of insulin, titrate up 1U every night until FPG is within 4-7mmol/L)

  1. Basal and bolus insulin
  2. Biphasic (premixed) insulin (RAIA + intermediate acting insulin)
218
Q

Why would insulin be initiated as basal only?

A

It is preferred for the following reasons:

Simplicity

Minimization of weight gain and hypoglycemia

Keeping oral agents on board helps with sensitization

219
Q

What is overbasalization in glucose control with insulin?

A

This occurs when a basal insulin dose of over 0.5U/kg/d, they get no additional benefits

If this patient seems like they need more insulin-like activity, consider other options rather than continuing to increase the basal insulin dose

220
Q

What are some options for when basal insulin are not doing the trick?

A

Evaluate/ add other antihyperglycemics (DDP4i, GLP1RA, SGLT2i)

Basal insulin/GLP1RA combos

Basal/bolus insulin

221
Q

How to initiate basal-bolus insulin?

A

If patient is okay with injecting insulin four times a day, then introduce one prandial insulin at a time

  1. Start with largest meal (2-4U)
  2. Titrate by 1-2U/week until FPG and PPG at target
  3. As insulin gets added, consider removing secretagogues
  4. Monitor for effectiveness (blood glucose targets) as well as hypoglycemia
222
Q

Review slides 283-285 for a great treatment algorithm for T2DM

A
223
Q

What are some factors pharmacists should consider when choosing a second line drug for T2DM?

A

After metformin, considerations to be made:

Clinical CV disease
Hypoglycemia
Affect on weight
Renal function
Degree of hyperglycaemia
Other comorbidities (HF)
Cost
Patient preference

224
Q

What is the mechanism of action for Tirzepatide?

A

It is a GIP and GLP1 dual agonist

Tirzepatide enhances the secretion of insulin in response to food and reduces glucagon

225
Q

What is the dosing for Tirzepatide?

A

Initiate at 2.5mg sc once weekly

Increase by 2.5mg increments every 4 weeks to max dose of 15mg

226
Q

What are some adverse effects associated with Tirzepatide?

A

Mostly GI

Nausea

Diarrhea

Vomiting

Dyspepsia, constipation, abdominal pain

227
Q

What is the potential for Tirzepatide in weight loss?

A

The SURPASS-4 study showed Tirzepatide to reduce body weight by 25.8lbs vs. 4.3lbs with glargine (LAIA)

228
Q

What are some concerns with Tirzepatide use?

A

Mean increase in HR of 2-4 BPM

Delays gastric emptying and could inhibit absorption of drugs that depend on GI motility
Ex. Oral contraception

229
Q

Can SGLT2 inhibitors and GLP1RAs be used in T1DM?

A

Not enough evidence for safety and efficacy

Risks outweigh benefits

230
Q

What is the traditional T2DM treatment strategy?

A

Can be described as treat to fail

T2DM diagnosis—> lifestyle —> metformin —> other oral agents —> insulin

231
Q

What is an alternate T2DM treatment strategy?

A

Induce glycemic remission (in early T2DM, it is thought it can be reversed back to normal glucose control)

Short-term insulin therapy (2-5 weeks) to modify disease and preserve beta-cell function

232
Q

What actions do women who want to get pregnant need to take to manage their diabetes and reduce risk?

A

Use reliable birth control until blood glucose is optimized

Aim for A1C of under 7% (under 6.5% if safe)

Poorly controlled diabetes increases the risk of miscarriage, stillborn, and malformations

Get ophthalmological assessment to assess retinopathy before, during, and after conception

Screen for CKD

233
Q

What medications can be used before pregnancy?

A

Preconception:
Folic acid for normal neural tube development

d/c potential embryopathic drugs (ACEi/ARB, Statins)

T1DM: Insulin
T2DM: Can continue metformin, Glyburide, or insulin

234
Q

What antihyperglycemics are safe for use during pregnancy?

A

Once pregnancy occurs, insulin is the drug of choice for both T1DM and T2DM

*Metformin and then Glyburide may be considered as alternatives for women unwilling to use insulin

235
Q

What are some treatment options for new-onset gestational diabetes?

A

First line: diet and exercise (if glycemic targets are not achieved in 2 weeks, start pharmacotherapy)

Second line: insulin (metformin and Glyburide are alternatives)

Screen for diabetes after pregnancy as well

236
Q

What are the advantages of breastfeeding in terms of glucose control?

A

It can reduce offspring obesity and for at least 4 months it can reduce the risk of developing diabetes (both mother and child)

237
Q

What is the risk of insulin to infants when they drink breast milk?

A

Insulin can be found in the breast milk, but it breaks down in the infants stomach before it can reach the infant’s systemic circulation

238
Q

What are some concerns with diabetes in children ?

A

Psychological risks (they are different, can be picked on)

Eating disorders

Insulin omission

Need access to a dietician

Smoking cessation

Contraception

239
Q

What are glucose targets for children with T1DM?

A

They are given intensive insulin whenever possible

A1C target of under 7-7.5% for all children under 18

FPG: 4-8mmol/L
2hr PPG: 5-10mmol/L

240
Q

What are some treatment options for T2DM in children?

A

Often need to address lifestyle for whole family

Individualize targets based on patient (A1C could be different)

Pharmacologic options:
Metformin (first line)
Metformin + basal insulin (for severe hyperglycaemia)
Metformin + Liraglutide (Liraglutide can be used instead of basal insulin)

241
Q

What are some treatment considerations for T2DM in elderly?

A

No two elderly patients are the same, so individualize targets

Need to consider fragility and risk of hypoglycemia (both increase fracture risk). Use DPP4is over SUs

Use a clock drawing test to gauge cognitive and dexterity ability to administer insulin accurately

242
Q

Review slide 302 for a more detailed chart of glycemic targets in older adults

A
243
Q

What are some acute diabetes-related complications?

A

Hypoglycemia (under 4mmol/L)

Hyperglycaemia (Diabetic ketoacidosis, Hyperglycemuic Hyperosmolar State)

Infections (Influenza, pneumonia, COVID-19)

244
Q

What are some chronic diabetes complications?

A

Macrovascular (CVD, Dyslipidemia, HTN)

MIcrovascular (Nephropathy, Retinopathy, Neuropathy)

Other Considerations (Diabetes and Mental Health, Obstructive Sleep Apnea, Diabetes and driving)

245
Q

What is the definition of hypoglycemia?

A
  1. Low blood glucose levels (under 4mmol/L)
  2. Development of autonomic (adrenergic) or neuroglyopenic (CNS) symptoms
  3. Symptoms respond to the intake of carbohydrates
246
Q

What are some common causes of hypoglycemia?

A

Not eating on time (missed meals or not eating enough)

Unusual amount (excessive) of physical activity

taking too much of an antihyperglycemic medication

Alcohol (mimics the symptoms of hypoglycemia)

Prior episode of severe hypoglycemia, hypoglycemia unawareness

247
Q

What are some autonomic symptoms associated with hypoglycemia?

A

When blood glucose falls below 4mmol/L, the following autonomic symptoms can develop:

TRembling

Palpitations

Sweating

Anxiety

Hunger

Nausea

TIngling

248
Q

What are some neuroglycopenic symptoms associated with hypoglycemia?

A

The following symptoms can develop after blood glucose levels fall below 2.8mmol/L:

Difficulty concentrating

Confusion

Weakness

Drowsiness

Vision changes

Difficulty speaking

Headache

Dizziness

249
Q

What are the different severity levels in hypoglycemia?

A

Mild (BG between 3.9-3.0mmol/L):
Autonomic symptoms present

Moderate (BG is between 3.0-2.8mmol/L):
Autonomic and neuroglycopenic symptoms present

Severe (BG is below 2.8mmol/L): In addition to autonomic and neuroglycopenic symptoms, they patient is likely to be unresponsive and unconscious.

250
Q

What are some major risk factors for severe hypoglycemia in T1DM?

A

Prior episode of severe hypoglycemia

Current low A1C (under 6.0%)

Hypoglycemia Unawareness (symptoms appear at more severe levels of hypoglycemia)

Long duration of diabetes

Autonomic neuropathy

Adolescence

Pre-schooled aged children that are unable to detect and/or treat hypoglycemia on their own

251
Q

What are some major risk factors for severe hypoglycemia in T2DM?

A

Advancing age

Severe cognitive impairment

Poor health literacy

Food insecurity

Increased A1C

Hypoglycemia unawareness

Duration of insulin therapy

Renal impairment

Neuropathy

252
Q

What exactly is hypoglycemia unawareness?

A

The inability to recognize the early warning signs of low blood glucose

The first symptoms experienced in hypoglycemia is confusion or loss of confusion

This develops due to frequent hypoglycemia

253
Q

What causes frequent hypoglycemia?

A

A decrease in the hormonal response mechanisms that prevent hypoglycemia (epinephrine and glucagon)

A lowering of the threshold at which hypoglycemia symptoms are experiences

Beta-blockers can contribute to hypoglycemia unawareness

254
Q

How to address hypoglycemia in general ?

A
  1. Recognize autonomic or neuroglycopenic symptoms
  2. Confirm if possible (with glucose monitoring devices)

3.Treat with “fast sugar” to relive symptoms

  1. Retest in 15 minutes to ensure blood sugar is above 4.0mmol/L, and retreat with “fast sugar” if needed
  2. Eat usual snack or meal due at that time of the day
255
Q

How is mild to moderate hypoglycemia treated specifically?

A
  1. Eat or drink 15g of “fast sugar” (will increase blood sugar by 2.0mmol/L in 20 min)
  2. Wait 15 min then check blood sugar again. If lower than 4.0mmol/L, then treat with 15g of “fast sugar” (15-15 rule)
  3. Once blood glucose is above 4.0mmol/L, eat within an hour
  4. Once blood sugar is above 5.0mmol/L, the patinet is safe to drive. This can take 40 min after the meal to achieve this blood sugar reading
256
Q

What are some “fast sugars” that can be used to reverse hypoglycemia?

A

These sources of sugar are rapidly absorbed as glucose:

4 glucose tabes (Dex4 tabs)

15mL of sugar dissolved in water

2/3 cup of juice or soft drink

6 Life Savers

15mL (1tbsp of honey)

257
Q

How is severe hypoglycemia treated in a conscious patient?

A

If the patient is conscious:
1. Treat with oral ingestion of 20g of “fast sugar” preferably as glucose tabs (will raise blood glucose by 3.5mmol/L over 45 min)

  1. Wait 15 min and retest blood glucose
  2. Retreat with another 15g of glucose if the blood glucose level remains under 4.0mmol/L
  3. Eat usual snack or meal due at that time of day
258
Q

How is severe hypoglycemia treated in an unconcious patient?

A
  1. Treat with glucagon (1mg IM or IV, or 3mg nasal spray): Triggers the release of stored sugar
  2. Call 911
  3. Turn the patient into recovery position
  4. Eat as soon as safely possibel
  5. Discuss with healthcare team
259
Q

How do injectable and nasal glucagon compare to each other?

A

The two products have different storage requirements, but they have similar efficacy and response time

260
Q

What is pseudo-hypoglycemia?

A

A state in which an individual experiences symptoms of hypoglycemia without blood sugar being below 4.0mmol/L

261
Q

Why does pseudo-hypoglycemia occur?

A

Usually occurs in patients who are accustomed to having chronic high blood glucose levels and have a rapid drop in blood glucose levels following diabetes’ treatment. HCPs still treat to take care of associated symptoms

Once blood glucose is properly managed, pseudo-hypoglycemia resolves

262
Q

What are some causes of HYPERglycaemia?

A

Too little or omission of insulin (if needed)

Illness (increased metabolic demands = more glucagon = more blood sugar needed to power everything)

Surgery

Injury

Stress (emotional or physical)

Increased dietary intake

Exercise (in T1DM)

263
Q

What is Diabetic ketoacidosis (DKA)?

A

DKA occurs as a result of insulin deficiency and is characterized by the following:

Hyperglycaemia (usually above 14mmol/L)

Metabolic acidosis (pH under 7.3 and/or serum bicarbonate under 15mmol/L)

264
Q

When does hyperglycaemia cause water loss?

A

When the patient also has insulin insufficiency, the kidneys will use SGLT transporters to pull glucose from the blood and into the urine. This movement of glucose into the urine causes more water to flow into the urine due to osmotic pressure

265
Q

Why does keto acidosis develop in hyperglycaemia?

A

In insulin deficiency and increases in catecholamines stimulate lipolysis (TG and FFA breakdown into ketone bodies). This breakdown produces cellular energy, but also results in an increased ketone concentration

Increased ketone concentration = causes acidosis

266
Q

What are some signs and symptoms seen in Diabetic ketoacidosis (DKA)?

A

The following symptoms are due to hyperglycaemic component of DKA:
Excessive thirst

Excessive urination

Fatigue/weakness

Blurred vision

Change in appetite

The following are symptoms of acidosis component of DKA:
Abdominal pain, nausea, vomiting

Air hunger

Fruity acetone breath

Hyperventilation (Kussmaul Respiration, body tries to exhale excess CO2 in blood in attempt to reduce blood glucose concentrations)

Confusion

267
Q

How is diabetic ketoacidosis treated?

A

Each hospital has their own protocol, but they have a general pattern.

  1. Replacement of fluid loss
  2. Replacement of K+
  3. Correction of metabolic acidosis
  4. If patient is in shock or blood pH is under 7, Sodium bicarbonate may be added
  5. Once blood sugar reaches 14mmol/L, IV glucose should be added to target of 12-14mmol/L to prevent pseudo-hypoglycemia
268
Q

What is Hyperosmolar hyperglycaemic syndrome (HHS)?

A

HHS is another type of complication due to hyperglycemia.

It is less common than DKA, predominately affects T2DM patients

Exacerbated by extremely high blood glucose, increased osmolality, significant dehydration, and minimal ketoacidosis

269
Q

Review slide 326 to review the differences in pathophysiology of DKA and HHS

A
270
Q

How is Hyperosmolar hyperglycaemic syndrome (HHS) managed?

A

Similar to DKA

  1. Fluid resuscitation
  2. Avoid hypokalemia
  3. Insulin administration
  4. Avoid rapidly falling osmolarity
  5. Find precipitating cause
271
Q

How can DKA and HHS be prevented in diabetes patients?

A

Education around sick day management (more likely to be hyperglycaemic when patient is sick)

Adjust insulin dose as needed, continue using insulin even when not eating

Frequent monitoring of blood glucose when ill

Check for ketones and make changes earlier

272
Q

Review slide 329 for the differences between Diabetic ketoacidosis and Hyperosmolar Hyperglycaemic Syndrome

A
273
Q

How do diabetic patients experience infections differently vs. non-diabetes patients?

A

People with diabetes are at a greater risk of morbidity and mortality from influenza, pneumonia, and COVID-19 infections

Therefore it is important that diabetes patients are up to date for their vaccination status

274
Q

Why are infections especially concerning for a diabetic patient ?

A

People with diabetes need to be mindful of their blood glucose levels and medications in periods of acute illness

  1. Illness is a stressor causing an exaggerated counter-regulatory hormone response (overproduction of glucose, FFAs, and ketones bc energy demands are greater when sick. Increased risk for hyperglycaemia)
  2. Illness may be accompanied by dehydration and decreased appetite (increased urination, vomiting, and diarrhea)
275
Q

How do d iabetes patients perform effective sick day management?

A

Monitor blood glucose more frequently (q2-4h)

T1DM: Continue insulin, but adjust bolus based on blood glucose (increase total daily dose by 10-20%)

T2DM: If patient uses insulin, they should Increase or decrease dose depending on self-monitoring blood glucose

Drink plenty of glucose-free fluids (water) to limit hyperglycemia and dehydration

If unable to eat solid food, substitute with glucose containing fluids

276
Q

Review slide 334 for a guideline on sick day management in diabetes

A
277
Q

What is SADMANS in terms of sick day management in Diabetes?

A

Diabetes patients are instructed to d/c the following medications when they are sick due to issues with kidney function decline and increased risk for adverse effects:

S(ulfonylureas)
A(CEi)
D(iuretics, direct renin inhibitors)

M(etformin)
A(RBs)
N(SAIDs)
S(GLT2 inhibitors)

278
Q

What is the relationship between CV disease and Diabetes?

A

Diabetes increases the risk of many CV diseases:

Heart Failure (2-4x higher risk and occurs at earlier ages)

Acute Coronary Syndrome (3x higher risk + 15 years sooner + 2x mortality risk)

Stroke (2-5x higher risk + 2x reoccurrence rate)

279
Q

Can increased CV risk due to Diabetes be reduced?

A

Yes, if the patient is able to successfully address risk factors

280
Q

What risk factors should be minimized to reduce risk of CV conditions in the context of Diabetes?

A

ABCDESSS is a useful acronym

A1C targets should be under 7.0%)
BP should be under 130/80
Cholesterol, LDL should be under 2.0mmol/L
Drugs for CVD risk reduction: ACEi/ARB, ASA, and SGLT2i/GLP1RA in T2DM
Eexercise and healthy Eating
Screening for complications (ECG every 3-5 years, Monofilament annually, eGFR and ACR annually, Retinal exam annually)
Smoking cessation
Self-management (Stress, mental health, financial, or other concerns that could be barriers to achieving goals)

281
Q

What is the prevalence of HTN in diabetes patients?

A

70% of Diabetes patients have hypertension

HTN is a major cause of microvascular and CV complications

Goal: 130/80 and should be checked at every appointment

Treatment: Lifestyle intervention and pharmacotherapy

282
Q

What are some first line drugs for patients with CVD, CKD, or with CV risk factors in addition to Diabetes and HTN?

A

ACEi or ARB

283
Q

What are some first line drugs for patients who have no CV risk factors, but have Diabetes and HTN?

A

ACEi, ARBs, DHP CCBs, TZDs

284
Q

Should every diabetes patient be on an ACEi or ARB even if blood pressure is normal?

A

No, only use ACEi or ARBs if patient has diagnosed HTN or CV risk factors (CVD, Age over 55 + a risk factor or target organ damage, Microvascular complication)

285
Q

What is the relationship between Diabetes and Dyslipidemia?

A

Most adults with diabetes are at greater risk for CV disease (MI and stroke)

Lipid profile should be performed at diagnosis and repeated annually

286
Q

How can diabetes patients reduce their CV risk in terms of contribution from Dyslipidemia?

A

Statins are recommended for almost all diabetes patients:

Age over 40
Age over 30 + diabetes duration of over 15 years
Microvascular disease

Goal: Reduce LDL to below 2.0mmol/L

287
Q

Do any antihyperglycemic agents confer any CV risk reduction?

A

Yes, GLP1RAs and SGLT2i can reduce CV risk

These agents offer CV risk reduction as a bonus in addition to reducing blood sugar

288
Q

How can diabetes patients limit the progression of microvascular complications?

A

Tight control of BP, BG, and lipids is key in preventing and/or delaying progression of microvascular complications

289
Q

How are diabetes and CKD related?

A

The primary cause of CKD in diabetes patients is diabetic nephropathy

Risk factors of diabetes nephropathy include:
Longer duration of diabetes

Poor BG, BP, and lipid control

Obesity

Smoking

290
Q

How often should renal function be screened in diabetes patients?

A

Random urinary ACR and a serum creatinine levels

T1DM: 5 years after diagnosis in adults
T2DM: At diagnosis

CKD can be diagnosed if eGFR drops by more than 60mL/min or ACR over 2.0mg/mmol on at least 2 of 3 samples over a 3 month period

291
Q

What patient groups should we avoid screening for CKD?

A

The following can increase ACR independent of kidney damage:

Exercise within 24h

Infection

Fever

HF

Marked hyperglycemia

Menstruation

Marked hypertension

292
Q

How is diabetic nephropathy treated?

A

Treatment is aimed to slow progression of kidney damage.

  1. Optimize blood glucose control
  2. Optimize blood pressure control (under 130/80)
  3. Use SGLT2i
293
Q

What is the relationship between diabetes and issues with vision?

A

Diabetic retinopathy is a vascular complication of diabetes. Caused by leaky retinal blood vessels due to damage form high BG and BP

Diabetic retinopathy is the most common cause of legal blindness among adults (20-70yo)

Diabetics also have higher rates of glaucoma and cataracts

294
Q

What are some risk factors for retinopathy?

A

Duration of diabetes

Glycemic control

HTN, Dyslipidemia

Anemia

Nephropathy

Tobacco use

African American

Pregnancy

295
Q

How should diabetic retinopathy be screened?

A

T1DM: 5 years after diagnosis after older than 15yo

T2DM: At diagnosis (then q 1-2yrs)

296
Q

How can diabetic retinopathy be prevented?

A
  1. Optimize glycemic control
  2. Optimize BP control
297
Q

What are some treatment options for diabetic retinopathy?

A

Varies on the type of ocular problem

Laser therapy, intraocular injections, vitreoretinal surgery

298
Q

What is diabetic neuropathy?

A

It is a type of nerve damage that can occur as a result of having diabetes.

Nerve damage most commonly results from reduced blood flow to nerves due to hyperglycemia-induced damage to blood vessels

It is a chronic and often progressive disease, early recognition and management is ideal

299
Q

What are the different types of diabetic neuropathy?

A
  1. Distal Sysmmetric Poly-Neuropathy (DSPN):
    Most common
    Involves the sensorimotor nervous system
  2. Diabetic Autonomic Neuropathy (DAN):
    Involves the autonomic nervous system
    Includes the heart, genitourinary system, sexual function, sudomotor abnormalities
300
Q

What are some risk factors for diabetic neuropathy?

A

Elevated BG

Elevated triglycerides

High BMI

Smoking

HTN

301
Q

How should diabetic neuropathy be screened for?

A

A clinician uses sensitivity to a micro filament to gauge level of neuropathy

T1DM: After 5 years post-pubertal duration (then annually)

T2DM: At diagnosis, then annually

302
Q

What are some effects of diabetic autonomic neuropathy on the GI tract?

A

Gastroparesis:
Delayed stomach emptying due to vagus nerve damage. This effectively slows or halts peristalsis, causing inconsistent food absorption and subsequent erratic BG levels

303
Q

What are some effects of diabetic autonomic neuropathy on the cardiovascular system?

A

Can cause resting tachycardia, exercise intolerance, orthostatic hypotension, silent MI, risk factor for mortality

304
Q

What are some effects of diabetic autonomic neuropathy on the genitourinary tract?

A

Bladder dysfunction

ED (affects 40% of men with diabetes, so ask about ED)

Retrograde ejaculation

305
Q

What are some effects of diabetic autonomic neuropathy on sexual function?

A

Women: Decreased vaginal lubrication, arousal, excitement, satisfaction, orgasm. Increased dyspareunia(pain before, during, and after sexual intercourse)

Men: Can experience ED

306
Q

What are some effects of diabetic autonomic neuropathy on metabolism?

A

Hypoglycaemia unawareness

Hypoglycaemia unresponsiveness

307
Q

What are some effects of diabetic autonomic neuropathy on sudumotor function (sweat glands)?

A

Gustatory sweating (during tasting)

Anhidrosis (reduced sweat production)

Heat intolerance

Dry skin

308
Q

What is peripheral neuropathy?

A

It is the most common type of neuropathy

Peripheral neuropathy will develop within 10 years of the onset of T1DM or T2DM in 40-50% of patients

Diabetes is the most common cause of peripheral neuropathy (presents in the feet first)

309
Q

What are the symptoms of Peripheral Neuropathy?

A

Early symptoms (small fibres affected):
Pain
Burning
Altered sense of temperature

Involvement of larger fibres:
Loss of protective sensation (LOPS)
Numbness

310
Q

How is peripheral neuropathy treated?

A

Optimize blood glucose:

Can be prevented in T1DM

Progression can be slowed in T2DM

311
Q

How is pain associated with peripheral neuropathy managed?

A

Oral agents:
Gabapentinoids (pregablin, gabapentin)
SNRIs (duloxetine, desvenlafaxine)
Na+ channel blockers (valproic acid)
TCAs (amitriptyline)

Topical:
Capsaicin (minimal effect)

Cognitive Behavioural Therapy

312
Q

Can pain management completely eliminate pain?

A

No, complete pain relief is usually not achieved. 30% of pain reduction is considered a success in clinical trials

Goal is to reduce,not to eliminate pain (improve quality of life)

313
Q

What is the role of foot care in diabetes?

A

Good foot care is an important component of diabetes management

Nerve damage as a result of diabetes makes one less likely to notice when feet are injured

314
Q

What factors that contribute to amputation in diabetes?

A

Nerve damage or diabetic neuropathy

Skin changes (non-healing ulcers due to nerve damage and reduced circulation)

Calluses

Smoking (increases the risk of non-healing ulcers)

Prolonged hyperglycaemia (causes neuropathy and poor circulation)

HTN (development of non-healing ulcers)

315
Q

How are the feet screened in diabetes?

A

Annual foot examinations including visual assessment, pedal pulses, and sensory foot exam with monofilament

316
Q

What are some good foot care habits to help prevent amputation?

A

Wash feet in warm water using a mild soap

Dry feet carefully, especially between toes (prevent fungal infections)

Check feet and in between toes to ensure no cuts, cracks, ingrown toenails, blisters

Clean cuts with mild soap and water, then cover with dressing

Trim toenails straight across and file any sharp edges

Apply unscented lotion to heels and soles (prevent cracking)

Don’t put lotion between toes since this can prevent infection

Wear clean socks and well-fitting shoes daily (do not go barefoot)

Test bath water temperature with your hand before you step in to make sure the water is not too hot

Avoid sitting for long periods of time

Do not smoke

317
Q

Review slide 377 on instructions on how to perform a monofilament exam for peripheral neuropathy

A
318
Q

What should pharmacists do for patients at risk for amputation due to peripheral neuropathy?

A

Educate about proper foot care (daily self exam and HCP at once yearly)

Pharmacists can perform monofilament assessments

Refer patients with foot ulcers and other complications to those specialized in foot care

319
Q

What is the relationship between diabetes and mental health?

A

10% of patients with diabetes will have major depression and 30% will experience clinical symptoms

Diabetes patients should be regularly screeds for diabetes-related psychological distress and psychiatric disorders

320
Q

What is the relationship between Obstructive Sleep Apnea and Diabetes?

A

18% of diabetes patients have sleep apnea

A lot of diabetes patients are obese, 86% of these individuals have sleep apnea

If a diabetes patient is having difficulties controlling their blood glucose and/or BP despite good adherence to lifestyle mods. and drug therapy. Their sleep apnea could be elevating their blood glucose and pressure

321
Q

What is T2DM remission?

A

Achieving specified A1C thresholds without any anti-hyperglycemic medications for a minimum for 3 months:

Remission to prediabetes (A1C between 6.0-6.4%)

Remission to normal glucose concentrations (A1C under 6.0%)

322
Q

What patients are qualified to undergo T2DM remission?

A

The patient is interested in attempting remission

Those who do not have significant eating or mental health disorders

Those who do not have a compelling indication for antihyperglycemics (for renal or CV benefit)

323
Q

What are some options for T2DM remission?

A

Bariatric surgery:
May induce remission in a non-pregnant adult with BMI over 35 (obese patients)

Health behaviour interventions:
Low-cal diets (800-850kcal/day) with meal replacement products for 3-5 months aimed at achieving more than 15kg weight loss

OR

Calorie-restricted diet (aim for 5-7% weight loss) and exercise (4-7 hours/week of structured physical activity spread over 5 days/week)

324
Q

Do most patients achieve their A1C targets after therapy?

A

A significant minority (38%) of patients are not able to achieve their A1C targets

325
Q

What is the role of a pharmacist in diabetes?

A

Education

Optimize therapy

Referrals to HCPs (direct patient towards getting help)

Help fill some of the gaps (prevent patients from slipping between the cracks of the healthcare system)

PHAR 152* (16 decks)

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